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Biomedical subjects

H Omran

Publications and source records attributed to H Omran.

86 records · Page 5Linked to original sources
PubMed1994

Reduction of cerebral blood flow with induced tachycardia in rats and in patients with coronary artery disease and premature ventricular contractions.

A reduction of cerebral blood flow (CBF) was observed in experimental studies in rats immediately after the onset of parasystolic rhythm or with stable, but haemodynamically compromising, tachycardias. Based on these data and with a view to studying the effects of premature ventricular contractions (PVCs) on the cerebral circulation in humans, CBF was measured using the 133-Xenon inhalation method in 24 age matched human controls (group A1: age 58.5 +/- 6.2 years; group A2: 52.2 +/- 7.8 years) in nine coronary artery disease (CAD) patients without PVCs (B), in 11 CAD patients with frequent PVCs (> 300.h-1) (C) and in nine patients, after exclusion of CAD by angiography, also with frequent PVCs (> 300.h-1) (D). Holter monitoring was performed during the CBF measurement. CBF determined in the human control groups A1 and A2 was 79.9 +/- 9.9 ml.100 g.-1 min-1 and 81.5-13.0 ml. 100 g-1 min-1, respectively. CBF was 74.1 +/- 13.6 ml . 100 g.-1 min-1 (P = 0.267 vs A1) in group B, 65.8 +/- 11.8 ml.100 g-1 min-1 (P = 0.004 vs A1) in group C and 74.2 +/- 15.6 ml.100 g.-1 min-1 (P = 0.218 vs A2) in group D. The significant reduction of CBF in CAD patients with frequent PVCs suggests that arrhythmias have a significant impact on CBF. Non-CAD patients with frequent PVCs did not show significant CBF decreases in comparison with controls. One can hypothetize that an impairment of electrical postextrasystolic potentiation, due to premature ventricular depolarization, and hence myocardial dysfunction leads to CBF reduction in CAD patients. The CBF reduction with CAD could also reflect concomitant coronary and cerebral arteriosclerosis.

Aged↗
PubMed1994

Myocardial and cerebral hemodynamics during tachyarrhythmia-induced hypotension in the rat.

BACKGROUND: The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension. METHODS AND RESULTS: MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias. CONCLUSIONS: The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.

Animals↗
PubMed1994

[Cerebral circulation in patients with dilated cardiomyopathy and aortic valve diseases].

The present study was performed in order to investigate the effect of dilated cardiomyopathy and severe aortic valve disease on cerebral blood flow. Cerebral perfusion was determined in 39 healthy volunteers representing two control groups of different age (77.7 +/- 8.7; 79.7 +/- 8.1 ml/100 g/min), in 7 patients with dilated cardiomyopathy (64.0 +/- 4.7 ml/100 g/min), in 11 patients with severe aortic stenosis (71.1 +/- 14.8 ml/100 g/min), and in 6 patients with severe aortic regurgitation (54.6 +/- 5.8 ml/100 g/min). Regional cerebral blood flow was measured with the 133Xenon inhalation method. Cerebral blood flow in severe aortic regurgitation patients (p = 0.006) was markedly and significantly reduced versus controls, whereas in dilated cardiomyopathy patients (p = 0.197) and in patients with severe aortic stenosis (p = 0.111) cerebral blood flow was not significantly reduced. A chronic adaptation of cerebral blood flow to the profound reduction of cardiac output is assumed in dilated cardiomyopathy patients. The collapsing pulse and the maximal reduction of mean arterial blood pressure in severe aortic regurgitation patients cause the reduction of autoregulatory capacity of cerebral blood flow with subsequent decrease of brain perfusion. Measurement of cerebral blood flow appears to be suitable for evaluation of perfusion deficits due to cardiac abnormalities. It provides an additional parameter for estimating the indication of valve replacement in patients with aortic valve disease.

Adult↗
PubMed1994

[Intermittent focal cerebral ischemia in hypotension due to pacemaker syndrome].

A pacemaker syndrome manifested as transient sensoric aphasia in a 68-year-old woman with a VVI-pace-maker implanted after SA-block. The attack occurred during long-term blood pressure recording and Holter monitoring. Borderline hypotension was documented during ventricular pacing which induced a retrograde excitation of the atrium. Clinical investigations excluded any intracranial abnormality, any source of embolism or stenosis of extra- and intracranial cerebral arteries. Cerebral blood flow measurements revealed a significant increase during pacing at elevated heart rate. Therefore, a device for AV-sequential pacing was implanted and basic pacing rate was elevated. The present case report indicates that focal and not only global cerebral ischemia can be produced by an impairment of systemic hemodynamics due to hypotension and a pacemaker syndrome. Improvement of cerebral blood flow during pacing is an unexpected finding contrasting with the concept of autoregulation. In addition, pacemaker implantation should be discussed in patients with transient cerebral perfusion deficits if an improvement of cerebral blood flow is documented along with rising heart rate.

Aged↗
PubMed1994

Echocardiographic profile of the normally functioning Omnicarbon valve.

Transthoracic echocardiography was performed in 141 patients with 90 Omnicarbon valves in the aortic and 66 in the mitral position. Additionally, 53 of them were investigated by transesophageal echocardiography comparing monoplane and multiplane facilities. The opening direction of the disc and the location of the pivot axis could be correctly determined by transthoracic, monoplane, and multiplane transesophageal echocardiography, respectively, in 100%, 80%, and 100% of the mitral and in 53%, 21%, and 82% of the aortic prostheses. Small regurgitation jets were detected in 90% of the aortic valves (1.6 +/- 0.4 cm2) by transthoracic and in all mitral prostheses (2.3 +/- 0.8 cm2) by transesophageal echocardiography. Based on morphological identification of the pivot points structures, origins of leakage jets were clearly identified as "design-related" in 12% (transthoracic echocardiography of aortic valves) to 100% (multiplane transesophageal echocardiography of mitral valves). In the aortic position, values obtained for transprosthetic forward flow velocity measurements exhibited wide scatter which did not allow a firm separation between valve sizes. No better differentiation was possible by using the calculated Doppler gradients or the velocity time integrals, either. Mean gradients and velocity time integrals showed even smaller differences between groups in the mitral valve patients. It is concluded that the Omnicarbon valve has a suitable design for morphological echocardiographic examination, and multiplane transesophageal technique expands the diagnostic capability. Forward flow measurements do not appear to be suited for detecting a beginning obstruction of this mechanical prosthesis.

Adult↗
PubMed1994

[Effect of nisoldipine and diltiazem on systolic and diastolic function of the left ventricle in patients with coronary heart disease].

OBJECTIVES AND BACKGROUND: Calcium channel blockers have a negative inotropic effect and protract the relaxation of the normal myocardium. These effects may vary in patients with coronary artery disease (CAD) and with the different kinds of calcium antagonists. In the present study we therefore compared the hemodynamic effects of intravenously given equihypotensive dosages of diltiazem (D) and nisoldipine (N) in patients with CAD. METHODS AND RESULTS: Each group contained 10 patients. After administration of a bolus of 300 micrograms/kg (D) and 5 micrograms/kg (N) respectively and following continuous infusion of 5.4 micrograms/kg/min (D) and 0.2 micrograms/kg/min (N) respectively, the mean arterial pressure was reduced by 15.5 +/- 6.0 (D) and 16.6 +/- 4.1 (N) mm Hg. Atrial pacing was performed in all patients to avoid reflectory heart rate effects. The pulmonary artery pressure decreased slightly with both drugs, whereas the cardiac index increased only with the use of N from 3.44 l/min x m2 to 3.93 l/min x m2. A significant change in the maximal rate of rise of left ventricular pressure (dP/dt max) as an index for inotropy was not detected for N or for D. The parameters of the diastolic function (the time constant of ventricular relaxation (tau) and the maximum rate of left ventricular isovolumic pressure decline (dP/dt min)) also did not indicate unequivocal drug effects. Doppler echocardiography of the mitral valve flow was performed simultaneously with invasive pressure measurements. The flow propagation derived from the color-M-mode correlated significantly with tau and was slightly improved by D.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

LODVIEW: a computer program for the graphical evaluation of lod score results in exclusion mapping of human disease genes.

For linkage analysis projects aimed at mapping hereditary disease genes in humans, hundreds of highly polymorphic microsatellite markers which can be typed by PCR (PCR markers) have become available. With this technical improvement, the availability of a technique allowing for transparency in the handling of rapidly generated lod score data is becoming important. We present a computer program LODVIEW for the graphical representation of lod score data. It is designed for the input of lod score data generated with the LINKAGE package or similar programs. LODVIEW consists of 24 preformatted files, one for each chromosome. Each file contains a table for the input of lod score data and a file for the graphical representation of the data, which will show automatically any entry that is made in the respective input table. The program provides the user with published PCR marker information pre-entered into a table and graph at the correct positions corresponding to the genetic distances between markers. The graphical display of LODVIEW allows for the rapid evaluation of lod score results calculated from PCR markers on each chromosome. The following information can be obtained from the graphical display at one glance: (i) Regions of exclusion (Z(theta) < -2) and nonexclusion, (ii) markers with positive lod scores, (iii) the distribution of positive and negative lod scores among the families examined (indication of genetic heterogeneity), (iv) multipoint lod scores, and (v) the availability of PCR markers in regions of interest. The program is continually updated for novel PCR marker information from the literature. The program will help to efficiently monitor and direct the progress of exclusion mapping projects.

Chromosome Mapping↗
PubMed1993

Mapping of a gene for familial juvenile nephronophthisis: refining the map and defining flanking markers on chromosome 2. APN Study Group.

Familial juvenile nephronophthisis (NPH) is an autosomal recessive kidney disease that leads to end-stage renal failure in adolescence and is associated with the formation of cysts at the cortico-medullary junction of the kidneys. NPH is responsible for about 15% of end-stage renal disease in children, as shown by Kleinknecht and Habib. NPH in combination with autosomal recessive retinitis pigmentosa is known as the Senior-Løken syndrome (SLS) and exhibits renal pathology that is identical to NPH. We had excluded 40% of the human genome from linkage with a disease locus for NPH or SLS when Antignac et al. first demonstrated linkage for an NPH locus on chromosome 2. We present confirmation of linkage of an NPH locus to microsatellite markers on chromosome 2 in nine families with NPH. By linkage analysis with marker AFM262xb5 at locus D2S176, a maximum lod score of 5.05 at a theta max = .03 was obtained. In a large NPH family that yielded at D2S176 a maximum lod score of 2.66 at theta max = .0, markers AFM172xc3 and AFM016yc5, representing loci D2S135 and D2S110, respectively, were identified as flanking markers, thereby defining the interval for an NPH locus to a region of approximately 15 cM. Furthermore, the cytogenetic assignment of the NPH region was specified to 2p12-(2q13 or adjacent bands) by calculation of linkage between these flanking markers and markers with known unique cytogenetic assignment. The refined map may serve as a genetic framework for additional genetic and physical mapping of the region.

Chromosome Mapping↗
PubMed1993

Semiquantitation of aortic regurgitation by pulsed Doppler examination of the subclavian artery velocity contour.

The reflux of aortic regurgitation causes an increased and longer diastolic reverse flow in the aorta and its branching vessels as compared to the normal flow contour. The changes of the aortic flow are related to the severity of aortic regurgitation and can be demonstrated by Doppler ultrasound. As Doppler examinations are often restricted in the aorta, a prospective study was designed to determine the feasibility and accuracy of Doppler measurements in the subclavian artery for the identification of severe forms of aortic regurgitation. Fifty-five patients with and 40 patients without aortic regurgitation were examined both by aortography and pulsed Doppler flow analysis of the subclavian artery. Two age groups were differentiated: patients below and those over 60 years of age, respectively. A high quality Doppler signal was recorded in all patients. In patients below 60 years, the best predictors of severe aortic regurgitation proved to be a pandiastolic reverse flow and an increased regurgitant fraction (77%) with a sensitivity of 100% and specificity of 75% and 92%, respectively. Since a pandiastolic reverse flow was detected in most patients in the control group over 60 years, it was not indicative of aortic regurgitation in these cases. However, an increased maximal diastolic velocity (> -37 cm/s) identified severe forms of aortic regurgitation in this age group with a sensitivity of 89% and a specificity of 100%. Therefore, severe forms of aortic regurgitation may be reliably identified by analysing the subclavian artery Doppler spectrum. In conclusion, the method is a useful adjunctive technique to other Doppler echocardiographic methods to assess the severity of aortic regurgitation.

Adult↗
PubMedDate not supplied

Multiplane transesophageal echocardiographic evaluation of transvenous defibrillation leads.

Permanent transvenous cardioverter-defibrillator leads were investigated by multiplane transesophageal echocardiography (TEE) (1) to determine whether intracardiac lead segments can be visualized, (2) to verify the position of the coils, and (3) to detect possible thrombus formation. The diagnostic information obtained in 62 patients by TEE was compared to that of transthoracic echocardiography (TTE). Abnormal findings were only visualized by multiplane TEE. However, further controlled studies are needed to determine the clinical relevance of displaced caval (one patient) and ventricular coils (15 patients), ventricular (1 patient) or atrial (6 patients) loops, and of clinically uneventful thrombi (13 patients).

Adult↗
PubMedDate not supplied

Morphology of the mitral valve as displayed by multiplane transesophageal echocardiography.

This study was performed to (1) describe how multiplane transesophageal echocardiography (TEE) facilitates imaging of the entire mitral valve apparatus, and (2) prospectively compare the morphology of the different segments of the mitral apparatus as determined by multiplane TEE and direct surgical inspection. The study consisted of 30 consecutive patients examined by multiplane TEE less than 24 hours before mitral valve surgery. The mitral valve was displayed in transgastric and transesophageal views with the imaging planes specifically aligned to demonstrate continuity between the papillary muscles, chordae tendineae, and leaflet edges. The character and location of morphologic abnormalities identified by findings of preoperative TEE were highly concordant with surgical inspection of the valve (p < 0.0001). Thus multiplane TEE offers the ability to visualize the entire mitral apparatus as a functional unit and to identify morphologic abnormalities of the valve correctly.

Adult↗
PubMedDate not supplied

The ontogeny of human gyrification.

During development the human cortex changes from a smooth lissencephalic structure to one that is highly convoluted. Increases in the degree of cortical folding are associated with brain size only for the first part of brain growth; during the second half, differences in cortical folding match those of brain size, resulting in no change in the degree of folding. When the degree of cortical folding is studied as a function of age, a brief postnatal overshoot, an effect of brain size, is observed. The analysis suggests that the mechanical hypothesis of cortical buckling can best explain the degree of cortical folding, but that other hypotheses, like gyrogenesis, are required to explain the placement and orientation of sulci. The adult asymptote in degree of cortical folding is associated with the onset and disappearance of single subplate lamina, suggesting that subplate:cortical plate associations should be examined as causal for gyrification. Areas whose sulci differ in length between the two hemispheres have similar degrees of convolutedness, supporting interpretations that the sizes of gyri are asymmetric in the two hemispheres. The ontogenetic data support the thesis that human cortical proportions evolved when the brain enlarged in size and that the process was not one of neoteny.

Adolescent↗
PubMedDate not supplied

Heart rate variability in patients with sleep-related breathing disorders.

The increased mortality among patients with obstructive sleep apnea syndrome has been explained in part by the increased incidence of arterial and pulmonary hypertension. A decreased heart rate variability (HRV) has been shown to be associated with an increased mortality as well. We investigated 53 patients, admitted to the hospital for chest pain for sleep-related breathing disorders (SRBD) with an ambulatory screening device (MESAM-IV). HRV was recorded simultaneously. All patients received coronary artery catheterization and 36 had significant coronary artery disease (CAD; 67.9%). Standard time domain parameters were compared by a 4-way Anova for patients with an oxygen desaturation index of more and less than 5/hour and the factors CAD, diabetes and beta-blocker use. The percentage of differences between RR intervals that differ more than 50 ms (pNN > 50: 9.0 +/- 11.1 vs. 19.2 +/- 22.2%: p < 0.05) as well as the root mean square of these differences (38.0 +/- 29.0 vs. 59.2 +/- 51.5 ms; p < 0.05) were significantly decreased in patients with SRBD. In an hourly breakdown the number of desaturations was not correlated with a change in HRV. Mean oxygen saturation was significantly decreased in patients with SRBD (95.2 +/- 1.8 vs. 96.2 +/- 1.42%, p < 0.05), and positively correlated with the pNN > 50 (r = 0.34, p < 0.01). This correlation might suggest a more profound pathophysiological interaction between HRV and SRBD than short-term vagal activation alone. The results favor HRV for inclusion in future risk stratification models in patients with sleep apnea syndrome.

Cardiac Catheterization↗