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Biomedical subjects

C Meissner

Publications and source records attributed to C Meissner.

At least 37 records · Page 2Linked to original sources
PubMed2000

Brain injury after gunshot wounding: morphometric analysis of cell destruction caused by temporary cavitation.

In addition to the primary destruction of brain tissue readily visible at autopsy (permanent track), gunshot wounding to the brain creates a pulsating temporary cavity due to radial expansion along the bullet's track. To determine the maximum extent of this temporary cavitation in brains of victims of gunshots from weapons with low muzzle velocity, we carried out morphometric studies on 20 cases of death from gunshot wounding to the head from bullets with a muzzle energy <500 J and a survival time of <90 min. The brains were fixed in formalin, examine macroscopically and microscopically, and subjected to morphometric analyses. Surrounding the permanent track, a narrow mantle-like zone of astrocyte destruction was found within an area of hemorrhagic extravasation. Axons near the permanent track had been broken into tiny fragments. The axonal damage lessened with increasing distance from the permanent track, although axons continued to be fragmented and to exhibit varicose changes and clumping until assuming their normal structure beyond 18 mm. Nerve cells were extremely shrunken close to the permanent track but gradually took on their normal shape with increasing distance. We also assessed the loss of glial fibrillary acid protein expression by astrocytes in the white matter, the extent of traumatic bleeding, and damage to axons and neurons as measured radially from the permanent track. Axonal and neuronal damage were found to extend about 18 mm radially from the permanent track, tapering gradually along the track from entry point to exit point. The destruction was probably produced by the temporary cavitation and accords with theoretical considerations and experimental observations.

Adult↗
PubMed2000

Mononuclear cells in subcutaneous haemorrhage with special consideration of myeloid percursor cells.

Various hematogenous markers were used to differentiate and quantify the types of mononuclear cells present in subcutaneous haemorrhages. Fifty samples of subcutaneous bleeding with a survival time of a few minutes to more than 48 hours were studied. The various cell types were detected using the following stains: Naphthol AS-D chloracetate esterase for myeloid cells, including mast cells; (alpha1-antichymotrypsin for monocytes/macrophages; UCHL1 for T-lymphocytes; and L26 for B lymphocytes. The percentage of monocytes/macrophages was found to increase in dependence on survival time, whereas T-lymphocytes declined. Within minutes of injury neutrophilic granulocytes had emigrated into the surrounding tissue and mast cell degranulation had occurred within the haemorrhagic zone. Esterase-positive mononuclear cells, namely metamyelocytes, were detected within minutes after injury and were still present after survival times exceeding 48 hours; however, no dependence on survival time or cause of death was found. Although the increasing number of monocytes/ macrophages and T-lymphocytes was expected, the sometimes high percentage of myeloid precursor cells within the wound were surprising. Possible explanations for this phenomenon are discussed.

Adolescent↗
PubMed2000

Petechiae of the baby's skin as differentiation symptom of infanticide versus SIDS.

The successive killing of three siblings by their biological mother at two-year intervals is described. The children were 367 days, 75 days and 3 years old. Although sudden infant death syndrome (SIDS) or interstitial pneumonia could not be ruled out as the cause of death in the two younger children, who were killed first, the third child exhibited discrete signs of violence in the mouth and throat area which were interpreted as proof of infanticide. All three children had petechiae of the skin of the face and throat, the upper thorax, the shoulders and the mucous membranes of the mouth. None of the children exhibited signs of a disease-related hemorrhagic tendency. After the mother was convicted of murdering the three-year-old boy by smothering in combination with compression of the thorax, she confessed to having killed the other two children in a similar manner. In the absence of hemostatic disease, the presence of petechiae of the skin extending over the entire drainage area of the Vena cava superior can be regarded as evidence of an increase in pressure in the thoracic cavity secondary to obstruction of the airways with simultaneous chest compression.

Asphyxia↗
PubMed2000

Sudden unexpected infant death due to fibroma of the heart.

A 7-month-old previously healthy female infant was found dead in her crib by her mother shortly after having been laid down to sleep following the noontime feeding. Because the child did not suffer from an acute illness and no other evidence pointed to a cause of death, it was initially assumed by the police that she had died of sudden infant death syndrome. At autopsy, however, the cause of death was determined to be cardiac arrhythmia secondary to fibroma of the heart.

Cause of Death↗
PubMed1999

Estimation of age at death based on quantitation of the 4977-bp deletion of human mitochondrial DNA in skeletal muscle.

The 4977-bp deletion in human mitochondrial DNA (mtDNA) is known to accumulate in various tissues with age. Since this deletion in mtDNA correlates closest with age in muscle tissue, iliopsoas muscle tissue was taken at autopsy from 50 persons aged 24-97 years to determine whether age at death can be estimated based on the amount of the 4977-bp deletion in skeletal muscle. Total DNA (nuclear and mtDNA) was extracted from 100 mg tissue and the 4977-bp deletion quantified using a kinetic polymerase chain reaction (PCR) followed by visualization of the products on silver stained polyacrylamide gels. The amount of the 4977-bp deletion of mtDNA ranged from 0.00049% to 0.14% depending on age, with a correlation coefficient of r = 0.83 (P = 0.0001). In forensic practice this method can aid in the estimation of age at death with a relatively wide confidence interval, thus enabling a discrimination between young and elderly persons in the identification of human remains based solely on skeletal muscle.

Acrylic Resins↗
PubMed1999

Is traumatic axonal injury (AI) associated with an early microglial activation? Application of a double-labeling technique for simultaneous detection of microglia and AI.

The aim of the present study was to determine whether axonal injury (AI) induces a microglial reaction within 15 days after brain trauma. In 40 selected cases of confirmed AI, the topographical relation of AI and microglial reaction was assessed using an immunohistochemical double-labeling technique for simultaneous demonstration of AI using beta-amyloid precursor protein (beta-APP) antibody and of microglia using CD68 antibody. Although traumatic injury was usually followed by a moderate early diffuse rise in the number of CD68-reactive cells in the white matter, increases in macrophages in areas of AI accumulation were only sporadic and did not occur until after 4 days. At survival intervals of 5-15 days a moderate microglial reaction in regions of beta-APP-positive injured axons was detected, at maximum, in half of the case material. During this interval AI-associated satellitosis-like clusters or stars described by other authors after a survival time of more than 7 weeks were an isolated phenomenon. The prolonged microglial reaction as well as the reduction of beta-APP-positive AI during longer survival periods supports the hypothesis that AI is not primarily chemotactically attractive and that the damage to a portion of beta-APPstained axons may be partly reversible. Most cases clearly require a prolonged interval of more than 15 days before initiation of the final scavenger reaction. For forensic purposes the increase in the number of microglial cells within the region of AI accumulation after a survival time of more than 5 days and the multiple and distinct demonstration of star-like microglial reactions within the white matter after survival times exceeding 7 weeks may provide valuable postmortem information on the timing of a traumatic event.

Adolescent↗
PubMed1999

Pontine axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain damage.

Experimental studies have shown that diffuse axonal injury is usually induced by positive or negative acceleration mechanisms. In order to determine the reliability of axonal injury (AI) as a marker of this type of traumatic insult, we compared cases of trauma-induced focal cortical hemorrhage without dural involvement (n = 67) with cases of trauma-induced subdural bleeding without cortical hemorrhage (n = 26). Both groups exhibited a wide range of post-traumatic survival times. The injuries in the first group were caused mainly by direct impact to the head, those in the second by acceleration/deceleration mechanisms. The investigations were based primarily on immunohistochemical demonstration of antibodies targeted to beta-amyloid precursor protein (beta-APP) in the pons as a marker of AI and the results were assessed semiquantitatively. No significant differences were found between the two groups. In both groups AI was detected in 80-100% of cases with survival times of more than 3 h and two thirds of all positive cases showed pronounced positivity. Additional comparison of cases of brain death due to mechanical trauma (n = 14) with cases of brain death due to non-mechanical trauma (n = 18) also disclosed no significant intergroup differences. Finally, investigations of the pons in cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the other groups, although the expression tended to be less pronounced. Our results confirm that beta-APP expression in the pons is a reliable indicator of AI but does not discriminate between injuries caused by traumatic strain or shearing mechanisms and secondary damage due to cerebral hypoxia/ischemia or edema. In the large majority of cases with prolonged post-traumatic survival, it can therefore be assumed that AI in the pons is the consequence of primary and/or secondary events or a combination of both, as is common in non-missile head injury survived for more than 90-120 min. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible.

Adolescent↗
PubMed1998

Demonstration of the 4977 bp deletion in human mitochondrial DNA from intravital and postmortem blood.

The 4977 bp deletion in mitochondrial DNA (mtDNA) is known to accumulate with age in various human tissues. Findings regarding its accumulation in blood, however, have so far been contradictory. We investigated the levels of the 4977 bp deletion in mtDNA from 100 intravital and postmortem blood samples. Applying an improved version of a PCR plus silver staining of polyacrylamide gels, we could detect the 4977 bp deletion in blood of healthy individuals over 20 years of age. While the 4977 bp deletion in blood is subject to a certain age dependence, it appears to be influenced by additional factors. A Primer-Shift-Assay amplifying four different deletion-specific fragments showed that the smaller fragments were amplified with a higher amplification efficiency than the larger fragments. The deletion-specific 389 bp fragment was demonstrated in 73% of individuals over 80 years of age, but in only 46% of individuals between 21 and 30 years old whereas the largest 802 bp deletion-specific fragment was detectable in 38% of subjects over 80 years of age, and in only 15% of individuals under 30 years of age. Deletion-specific fragments were not detected in a single individual under 20 years old, nor in fetal blood. In this work, we demonstrate for the first time the detection of 4977 bp specific fragments in blood of healthy individuals without the necessity of using a nested PCR. The deletion is detectable in postmortal and intravital blood, so that the occurrence of the 4977 bp deletion seems to be a physiological and not only a postmortal process.

Adult↗
PubMed1998

Axonal injury--a diagnostic tool in forensic neuropathology? A review.

We used beta-amyloid precursor protein (beta-APP) to investigate our own forensic neuropathological case material (n = 252) in light of the current literature on the phenomenon "axonal injury" (AI) to determine the incidence, specificity and biomechanical significance of AI and its significance for determining vitality and survival time. The case material consisted of cases of fatal nonmissile closed-head injury (n = 119), gunshot injury (n = 30), fatal cerebral ischemia/hypoxia (n = 51), brain death caused by mechanical trauma (n = 14) or nonmechanical injury (n = 18), and acute hemorrhagic shock (n = 20). AI was observed in 65% to 100% of cases of closed-head injury, fatal cerebral ischemia/hypoxia, and brain death with a survival time of more than 3 h; AI could not be detected in the cases of acute hemorrhagic shock. A statistically significant difference between traumatically and nontraumatically induced (nondisruptive) AI was not found. There was no statistical evidence of a correlation between AI and the different types of external force, since AI could be demonstrated after both acceleration/deceleration injuries and traumatic impact. Therefore, biomechanical inferences for reconstruction purposes are not possible. On the other hand, beta-APP was found to be a definite marker of vitality. In our material, cases with a posttraumatic interval of under 180 min did not express beta-APP. Moreover, the literature shows that the posttraumatic interval can be determined by other methods for demonstration of AI such as by ubiquitin immunostaining (360 min), silver staining (15-18 h), hematoxylin and eosin staining (about 24 h), or by demonstration of a microglial reaction (about 4 to 10 days) or of a few remaining isolated bulbs, without accompanying fibers, which can be detected after a survival time of up to 17 months.

Adolescent↗
PubMed1998

Enhanced reactivity of Alz-50 antibody in brains of sudden infant death syndrome victims versus brains with lethal hypoxic/ischemic injury. Diagnostic significance after application of the ImmunoMax technique on routine paraffin material.

Alz-50 antibody is immunoreactive with brain tissue of subjects with Alzheimer's disease and can also be demonstrated by immunocytochemistry in neurons of vibratome-prepared brain tissue of victims of sudden infant death syndrome (SIDS). The application of a slightly modified ImmunoMax method enabled us to demonstrate Alz-50 immunoreactivity in paraffin-embedded material. The Alz-50 epitope was detected in the hippocampus region and in nuclei of the medulla oblongata at the level of the inferior olivary protuberance in three diagnostic groups: victims of SIDS (n = 10), infants dying of subacute hypoxia/ischemia with subsequent (re-)perfusion (n = 9), and infants dying of acute ischemia without (re-) perfusion (n = 7). Quantitative evaluation of the hippocampal cortex and the nucleus olivaris inferior disclosed a significantly (P < 0.05) higher percentage of Alz-50-reactive neurons in SIDS cases than in the control groups (hippocampal cortex and the nucleus olivaris; SIDS victims: median = 100%; subacute hypoxia/ischemia: median = 33.6-81%; acute ischemia: median = 89.2-99%). Semiquantitative analysis revealed an equally pronounced preponderance of Alz-50-reactive neurons in SIDS victims versus the control groups. This greater expression in SIDS victims may be due to an ongoing hypoxia/ischemia during agony, but the present paucity of knowledge prohibits definitive elucidation. Nevertheless, the method described here appears to offer the realistic possibility of distinguishing SIDS cases from cases of sudden death in infants due to other causes, i.e., it offers for the first time a positive criterion for the diagnosis of SIDS.

Age Factors↗
PubMed1997

Detection of the age-dependent 4977 bp deletion of mitochondrial DNA. A pilot study.

In recent years a number of mitochondrial DNA (mtDNA) deletions have been detected in various tissues from individuals over 20 years of age. It has been postulated that these deletions are associated with natural aging. In order to determine whether a correlation exists between age and the amount of deleted 4977 bp mtDNA, we used two PCR reactions to study total DNA (nuclear and mitochondrial DNA) extracted from skeletal muscle (m. iliopsoas) obtained at autopsy from 93 individuals representing a wide age spectrum (range: 3 months-97 years). The primer pair L15/H15 was used to amplify a 533 bp fragment of intact mtDNA to determine the percentage of total DNA. A second PCR with the primer pair L35/H35 was then employed to amplify a 667 bp fragment of the deleted mtDNA. The amount of template DNA necessary to amplify the specific fragments of deleted mtDNA was found to decrease with age. Whereas no 4977 bp deletion could be detected in subjects under 20 years of age even with 1000 ng of total DNA, in individuals aged 21 to 30 years 1000 ng total DNA were sufficient. Only 1 ng total DNA was needed in all individuals over 70. Our results show that the 4977 bp deletion can be a useful marker of natural aging in human subjects.

Adolescent↗
PubMed1996

Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse.

Neuropathological studies were carried out on 180 human immunodeficiency virus-seronegative intravenous drug addicts. The findings in victims of acute heroin intoxication (n = 116) were congestion (99.1%), capillary engorgement (68.1%), and/or perivascular bleeding (68.1%) - hemodynamic processes attributable to toxic primary respiratory failure. In a high percentage of these cases (88%), cerebral edema was also present. In 18 cases of acute heroin intoxication who survived for periods of hours or days, the sole postmortem finding was ischemic nerve cell damages, resembling that typically seen in systemic hypoxia. Semiquantitative analysis revealed nerve cell loss in the hippocampal formation and/or Purkinje cell layer in 26% of the 162 chronic drug abusers. By contrast, in nearly 80% of these cases, the hippocampus showed enhanced expression of glial fibrillary acid protein by astrocytes and/or a proliferation of microglia, demonstrated by CD68 expression. Since such reactive processes are produced by primary neuronal damages, it can be assumed that chronic intravenous drug abuse results in obviously ischemic nerve cell loss. This could be demonstrated in the hippocampus, but it must also occur throughout the whole brain. The demonstration of ischemic nerve cell damage and neuronal loss or secondary reactive alterations has not been described previously.

Adolescent↗
PubMed1996

Activation of human neutrophils after contact with cellulose-based haemodialysis membranes: intracellular calcium signalling in single cells.

PURPOSE OF STUDY: In vitro contact of human leukocytes with cellulose-based dialysis membranes under complement-independent conditions results in activation of various leukocyte functions. To analyse signals involved in the mechanism of cell activation, we measured changes in cytosolic free calcium ([Ca2+]i) in individual human blood neutrophils (PMN) upon contact with flat sheet haemodialysis membranes. RESULTS: By confocal laser-scanning microscopy (CLSM), changes in [Ca2+]i were monitored in Fluo-3-labelled cells up to 10 min after contact with a regenerated cellulose (RC) membrane. Multiple [Ca2+]i transients were observed for cells in contact with RC; biostochastic analysis showed that up to 67% of the PMN responded with a high increase in [Ca2+]i, the rest were low- or non-responding cells. After contact with the new synthetic polycarbonate-polyether (PC-PE) membrane only non-responding cells were seen, indicating reduced cellular contact activation. The increase in [Ca2+]i of cells on RC could be inhibited by 5mM L-fucose. This monosaccharide was recently found to be present in cellulose-based polymers in picomolar concentrations. CONCLUSIONS: The data supports the hypothesis that dialysis-membrane-associated L-fucose residues participate in complement-independent leukocyte activation during haemodialysis therapy.

Biocompatible Materials↗
PubMed1996

Laminin mediates basement membrane induced differentiation of HEC 1B endometrial adenocarcinoma cells.

In vitro studies on endometrial carcinogenesis have been hampered by limited differentiation of the cells in culture. Using the endometrial carcinoma cell lines HEC 1B and its subclone HEC 1B(L), we established and characterized cell culture conditions that preserve a more differentiated state of the tumor cells. Randomly seeded HEC 1B(L) cells, if grown in a serum-free defined medium on top of a reconstituted basement membrane (Matrigel), within a few hours assembled themselves to web-like structures. In a thick layer of Matrigel, they showed an even more pronounced morphological differentiation. Functionally, two additional secretory proteins, about 31 and 77 kDa in size, became apparent as a response to matrigel. To further investigate the regulatory role of the extracellular matrix in the process of in vitro differentiation of endometrial adenocarcinoma cells, we addressed two specific problems. First, we investigated if the capacity of in vitro differentiation is a specific feature of HEC 1B(L) cells or if it is common to all endometrial adenocarcinoma cells. Second, we tried to identify the Matrigel component(s) responsible for in vitro differentiation. The assembly of HEC 1B and HEC 1B(L) cells into spatially organized web-like structures and the expression of the 77 kDa protein were thereby used as an assay. All endometrial adenocarcinoma cell lines tested to a variable degree formed web-like structures on Matrigel. Although the pattern of de novo synthesized secretory proteins changed as a response to Matrigel, only HEC 1A, HEC 1B, HEC 1B(L), and Ishikawa cells responded to culture on Matrigel by an increased expression of the 77 kDa protein. Functionally, polyclonal anti-laminin antibodies, but not anti-collagen type IV antibodies, disrupted formation of web-like structures by HEC 1B cells. The laminin-specific peptides YIGSR and SIKVAV but none of the RGD-peptides RGDS, GRGDSP, or GRADSP affected the three-dimensional assembly of these cells in vitro. Both anti-laminin antibodies and laminin-specific peptides suppressed Matrigel-induced formation of the 77-kDa secretory protein by HEC 1B cells. These findings suggest the involvement of laminin in the in vitro differentiation of the HEC 1B endometrial adenocarcinoma cell line. In a mechanistic view, laminin appears to play a crucial role in the regulation of this in vitro differentiation process.

Adenocarcinoma↗
PubMed1995

L-fucose residues on cellulose-based dialysis membranes: quantification of membrane-associated L-fucose and analysis of specific lectin binding.

Contact of mononuclear human leukocytes with cellulose dialysis membranes may result in complement-independent cell activation, i.e. enhanced synthesis of cytokines, prostaglandins and an increase in beta 2-micro-globulin synthesis. Cellular contact activation is specifically inhibited by the monosaccharide L-fucose suggesting that dialysis membrane associated L-fucose residues are involved in leukocyte activation. In this study we have detected and quantitated L-fucose on commercially-available cellulose dialysis membranes using two approaches. A sensitive enzymatic fluorescence assay detected L-fucose after acid hydrolysis of flat sheet membranes. Values ranged from 79.3 +/- 3.6 to 90.2 +/- 5.0 pmol cm-2 for Hemophan or Cuprophan respectively. Enzymatic cleavage of terminal alpha-L-fucopyranoses with alpha-L-fucosidase yielded 7.7 +/- 3.3 pmol L-fucose per cm2 for Cuprophan. Enzymatic hydrolysis of the synthetic polymer membranes AN-69 and PC-PE did not yield detectable amounts of L-fucose. In a second approach, binding of the fucose specific lectins of Lotus tetragonolobus and Ulex europaeus (UEAI) demonstrated the presence of biologically accessible L-fucose on the surface of cellulose membranes. Specific binding was observed with Cuprophan, and up to 2.6 +/- 0.3 pmol L-fucose per cm2 was calculated to be present from Langmuir-type adsorption isotherms. The data presented are in line with the hypothesis that surface-associated L-fucose residues on cellulose dialysis membranes participate in leukocyte contact activation.

Acrylic Resins↗
PubMed1995

The potential role of bacterial superantigens in the pathogenesis of Kawasaki syndrome.

Kawasaki syndrome is an acute multisystem vasculitis of infancy and early childhood associated with high fever, mucocutaneous inflammation, and the development of coronary artery abnormalities. Despite the widely held belief that Kawasaki syndrome is an infectious disease, investigations have failed to identify a causal organism. Previous studies have demonstrated that this illness is associated with marked activation of monocyte/macrophages and the selective expansion of V beta 2-, less so, of V beta 8.1/8.2-expressing T cells in the peripheral blood from Kawasaki syndrome patients during the acute phase of their illness. These immunologic features are characteristic of diseases that are caused by bacterial toxins which act as superantigens. Staphylococcal enterotoxins and streptococcal exotoxins are prototypic superantigens which stimulate large populations of T cells expressing particular T-cell receptor beta-chain variable (V beta) gene segments. Using the V beta 2+ T-cell expansion as an "immunologic footprint" for a superantigen, we have extended these observations to the identification and isolation of a novel clone of toxic shock syndrome toxin-1-producing Staphylococcus aureus in the majority of patients with Kawasaki syndrome and streptococcal pyrogenic exotoxin B/streptococcal pyrogenic exotoxin C-producing streptococci in a minority of Kawasaki syndrome patients. Toxic shock syndrome toxin-1, streptococcal pyrogenic exotoxin B, and streptococcal pyrogenic exotoxin C are known to stimulate V beta 2+ T cells. These observations support the hypothesis that the activation of V beta 2+ T cells during the acute phase of Kawasaki syndrome is caused by bacterial superantigen(s).

Autoimmune Diseases↗
PubMed1995

[Estimation of acute left ventricular afterload alterations. Transesophageal echocardiography in artificially respirated patients].

UNLABELLED: Left ventricular afterload is most accurately represented by left ventricular end-systolic wall stress, but in clinical practice is commonly estimated by the systemic vascular resistance (SVR). End-systolic wall stress can be derived from M-mode and two-dimensional (2D) echocardiograms in combination with systolic arterial pressure (SAP). We tested transoesophageal echocardiography for the assessment of acute left ventricular afterload alterations in ventilated patients requiring cardiovascular support with noradrenaline or nitroglycerine. METHOD. With approval from the local ethics committee, we studied afterload alterations in 11 hypotensive patients who were treated by increasing the dosage of i.v. noradrenaline by 2-5 micrograms/min in order to raise mean arterial pressure (MAP) by 20 mmHg. In another 10 patients with MAP over 95 mmHg, nitroglycerine was raised from 2 to 4 mg/h, aiming at a 20 mmHg MAP reduction. MAP and SAP were monitored via a radial artery cannula, cardiac output (CO) was measured with the thermodilution technique using a Swan-Ganz catheter, and SVR was calculated from CO, MAP, and right atrial pressure. M-mode and 2D echocardiograms were obtained from the cross-sectional short-axis view of the left ventricle and recorded shortly before and during treatment when MAP had changed by 20 mmHg. Left ventricular total area (TA) and cavity area (A) including the papillary muscles were obtained from end-systolic 2D echocardiograms, while end-systolic internal diameter (ID) and posterior wall thickness (HW) were measured in the M-mode. Wall stress was calculated in the M-mode as: WSM = 0.33 x SAP x ID/(HW x (1+HW/ID)), and in the 2D mode as: WS2D = 1.33 x SAP x A/(TA-A). STATISTICS: paired t-test (P < 0.05), regression analysis. RESULTS. Afterload alterations were reflected by significant changes of WS2D (-41%, +68%), WSM (-26%, +38%), and SVR (-15%, +50%). WSM and SVR underestimated changes of WS2D by 15%-30%. WSM changes due to SAP rather than to left-ventricular dimensional changes. No correlation was found between WS2D or WSM and SVR. Inter-observer variability for echocardiographic wall stress was reasonable (WS2D 4%, WSM 10%). CONCLUSIONS. Acute changes of left ventricular afterload and dimensions were clearly indicated by 2D measurements. As M-mode measures were not conclusive for left ventricular dimensional changes, WSM was not an appropriate parameter for acute afterload alterations. WS2D is an afterload index superior to WSM that cannot be estimated by SVR.

Blood Pressure↗