Dynamics in thrombus formation.
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Arterial Occlusive Diseases↗
Biomedical subjects
E Falk
Publications and source records attributed to E Falk.
Why do plaques rupture?
Rupture of the plaque surface, often with thrombosis superimposed, occurs frequently during the evolution of coronary atherosclerotic lesions. It is probably the most important mechanism underlying the sudden, rapid plaque progression responsible for acute coronary syndromes. The risk of plaque rupture depends on plaque type (composition) rather than plaque size (volume), because only plaques rich in soft extracellular lipids are vulnerable (rupture-prone). Most ruptures are tiny, occurring at the periphery of the fibrous cap that covers the lipid-rich core--points where the cap is usually thinnest and most heavily infiltrated by macrophage foam cells. Compared with intact caps, ruptured ones usually have less tensile strength and are more extensible, containing less collagen and glycosaminoglycans, more extracellular lipid, fewer smooth muscle cells, and more macrophages. Progressive extracellular lipid accumulation (lipid core formation) and cap weakening (macrophage related?) predispose the plaque to rupture and determine the actual vulnerability, which may change with time. Luckily, the plaque components responsible for vulnerability (soft lipid and probably macrophages) are apparently most likely to regress with treatment. The dynamic interplay between the actual plaque vulnerability and external stresses ("triggers") probably determines the particular moment and point of rupture, if this occurs. Vulnerability probably plays a more important role in rupture than triggers, because exercise stress testing of patients with advanced coronary artery disease rarely triggers a rupture/thrombus-related acute heart attack. A prerequisite is the presence of a vulnerable plaque.
Aging↗
[Dermatological laser treatment].
This article reviews the different lasers used in dermatology. Special emphasis is placed on the treatment of naevus flammeus ("portwine stain") where lasers are the treatment of choice. Argon laser and pulsed dye laser are the main lasers used in vascular skin diseases, and the article focuses on these two types. Copper vapour laser, neodymium-YAG-laser and CO2-laser are also presented. Information is provided about the availability of laser technology in the different health regions in Norway.
Adult↗
Coronary thrombosis: pathogenesis and clinical manifestations.
The majority (greater than 75%) of major coronary thrombi are precipitated by a sudden rupture of the surface of an atherosclerotic plaque (plaque fissuring) causing platelet aggregation where thrombogenic subendothelial tissue has been exposed. Whether the thrombus remains mural and limited, just sealing the rupture, or evolves into an occlusive thrombus seems to depend on: (1) the amount and character of exposed thrombogenic material; (2) the actual thrombotic-thrombolytic equilibrium; and (3) local flow disturbances due to preexisting atherosclerotic stenosis. Thrombus formation may take place within the stenosis, where blood velocity and shear forces are highest, or it may take place or extend poststenotically, where flow separation, recirculation, and turbulence prevail. Platelet aggregation within the stenosis is responsible for the primary flow obstruction, but fibrin subsequently enmeshes the platelets and thus stabilizes the thrombus. Most thrombi have a layered structure, indicating an episodic growth that may alternate with thrombus fragmentation and peripheral embolization: thrombosis and thrombolysis are dynamic processes occurring simultaneously. If the platelet-rich thrombus at the rupture site evolves into an occlusive thrombus, the blood proximal and distal to the occlusion may stagnate and coagulate, giving rise to a secondarily formed red stagnation thrombosis consisting predominantly of erythrocytes held together by fibrin membranes. A ruptured plaque with a dynamic thrombosis superimposed (with or without spasm) seems to underlie the great majority of acute ischemic syndromes: unstable angina, acute infarction, and sudden death. The clinical presentation and the outcome depend on the severity and duration of ischemia: whether the obstruction is occlusive or nonocclusive, transient or persistent--modified by the magnitude of collateral flow.
Coronary Artery Disease↗
Photoaffinity labeling of leukotriene binding sites in hepatocytes and hepatoma cells.
The method of direct photoaffinity labeling in the frozen state using the leukotrienes as suitable photolabile compounds may serve to identify and characterize polypeptides which interact with these eicosanoids during their hepatobiliary transport and metabolism. Furthermore, it will be a helpful technique to evaluate changes in the cell-specific protein pattern during neoplastic dedifferentiation of hepatocytes.
Affinity Labels↗
Fatal thrombosis of the basilar artery due to a minor head injury.
A case is reported where a 20-year-old alcohol-intoxicated man was admitted to the hospital after a minor head injury. Initially there was no neurologic disturbances or complaints but after a few hours he became comatose, and he died 4 days later without regaining consciousness. The autopsy revealed no lesions of the upper cervical spine or the vertebral arteries, but the basilar artery was occluded in its entire length. No traumatic lesions could be seen by naked eye examination of the artery, and there was no accompanying subarachnoid haemorrhage. A thorough microscopic examination, however, using step-sectioning technique revealed a significant incomplete arterial rupture with an occluding luminal thrombosis superimposed, consisting predominantly of aggregated platelets. Only the very thin adventitia separated the vascular lumen from the subarachnoid space preventing the more well known fatal complication to a minor head injury: A subarachnoid haemorrhage. To the best of our knowledge, fatal thrombosis of the basilar artery due to a minor head injury has not previously been reported. The pathogenetic mechanism seems to be identical to that underlying fatal subarachnoid haemorrhage following a similar trauma apart from the resulting arterial rupture being incomplete instead of complete.
Adult↗
Direct photoaffinity labeling of leukotriene binding sites.
Due to their conjugated double bonds the leukotrienes themselves are photolabile compounds and may therefore be used directly for photoaffinity labeling of leukotriene binding sites. Cryofixation eliminates unspecific labeling taking place in solution by photoisomers and photodegradation products of leukotrienes. After fixation of receptor ligand interactions by shock-freezing of the samples, irradiation-induced highly reactive excited states and/or intermediates can form covalent bonds with the respective binding site in the frozen state. After cryofixation of a solution of albumin incubated with [3H8]leukotriene E4, irradiation at 300 nm resulted in time-dependent incorporation of radioactivity into the protein. Photoaffinity labeling of rat as well as of human blood serum with [3H8]leukotriene E4 after cryofixation revealed that only one polypeptide with an Mr of 67,000 was labeled. This polypeptide was identified as albumin. Photoaffinity labeling of rat liver membrane subfractions enriched with sinusoidal membranes resulted in the labeling of a polypeptide with an apparent Mr of 48,000, whereas no polypeptide was predominantly labeled in the subfraction enriched with canalicular membranes. Photoaffinity labeling of isolated hepatocytes disclosed different leukotriene E4 binding polypeptides. In the particulate fraction of hepatocytes a polypeptide with an apparent Mr of 48,000 was labeled predominantly, whereas in the soluble fraction several polypeptides were labeled to a similar extent. One of these, with an apparent Mr of 25,000, was identified as subunit 1 of glutathione transferases by immunoprecipitation. The method of direct photoaffinity labeling in the frozen state after cryofixation using leukotrienes as photoactivatable compounds, as exemplified by leukotriene E4, may be most useful for the identification and characterization of various leukotriene binding sites, including receptors, leukotriene-metabolizing enzymes, and transport systems.
Animals↗
Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes.
Unstable angina appears to be a good clinical marker for rapidly progressing coronary artery disease. Pathologically, an unstable atherothrombotic coronary lesion, represented by a raised atherosclerotic plaque with ruptured surface causing variable degree of hemorrhage into the plaque and luminal thrombosis (rapid plaque progression), usually is present in patients at autopsy after a period of unstable angina. The thrombus at the rupture site may be mural and limited (just sealing the rupture) or occlusive, depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less than 75% stenosis (histologic cross-sectional area reduction), but it is found with increasing frequency when severity of stenosis increases beyond 75%. Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits, and microemboli/microinfarcts are frequently found in the myocardium downstream to coronary thrombi, indicating intermittent thrombus fragmentation with peripheral embolization. Such a "dynamic thrombosis" (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other thrombus-related acute coronary events: myocardial infarction or sudden death. Accordingly, progression of unstable angina to myocardial infarction or sudden death should, in principle, be preventable by the correct timing of current available therapies aimed to prevent or eliminate (1) the chronic atherosclerotic obstruction, (2) the acute plaque disruption, (3) luminal thrombosis, and (4) vasospasm.
Angina Pectoris↗
Prognostic significance of right ventricular infarction diagnosed by ST elevation in right chest leads V3R to V7R.
The prognostic significance of electrocardiographic "extensive right ventricular infarction" diagnosed by ST elevation greater than or equal to 1 mm in right chest leads V3R to V7R during inferior/posterior infarction was evaluated in 158 consecutive patients with first anterior (n = 72) or inferior/posterior (n = 86) myocardial infarction. At follow-up the maximum observation time was 3.0 years (mean 1.8 years). A total of 49 patients died; 96% due to cardiac causes. Twelve patients (8%) died during the first 24 hours of admission. Ten-day mortality was 18% (n = 29). Using Cox multivariate analysis ST elevation in right chest leads during inferior/posterior infarction was an independent predictor of prognosis in patients surviving the initial 10 days after infarction (n = 129). For these patients the cumulative survival was better after inferior/posterior infarction with ST elevation in V3R to V7R (n = 25) compared with (1) inferior/posterior infarction without St elevation in these leads (n = 45, P = 0.09), (2) anterior infarction (n = 59, P = 0.08), and (3) all other infarctions (n = 104, P = 0.05). Infarct size estimated by the peak serum enzyme values was similar in these groups. Thus, electrocardiographic extensive right ventricular infarction predicts a good prognosis in patients alive 10 days after infarction. Compared with infarcts of similar size but with another location the prognosis is better, probably due to concomitant smaller left ventricular infarction with better left ventricular function following infarction.
Adult↗
Right ventricular infarction: larger enzyme release with posterior than with anterior involvement.
To evaluate whether the right ventricle releases significant amount of cardiac enzymes during myocardial infarction, a clinicopathologic study of 50 patients with 60 infarcts was performed. Myocardial infarct size was determined at autopsy and compared with the corresponding peak serum lactate dehydrogenase and aspartate aminotransferase. Anterior and posterior infarcts had similar anatomic size, peak enzyme values, and coefficients of correlation (r = 0.86-0.88 versus r = 0.82-0.84 for lactate dehydrogenase). However, by disregarding the right ventricular infarct component considering the left ventricular infarction only, the coefficient of correlation between infarct size and peak serum lactate dehydrogenase decreased from r = 0.84 to r = 0.59 (P = 0.09), in 14 posterior infarcts while no change was observed in 24 anterior infarcts (r = 0.88). This indicates, that a considerable amount of enzymes released during posterior infarction originated from the right ventricle which was not the case for anterior infarction.
Aspartate Aminotransferases↗
Right ventricular infarction: diagnostic accuracy of electrocardiographic right chest leads V3R to V7R investigated prospectively in 43 consecutive fatal cases from a coronary care unit.
The accuracy of ST elevation greater than or equal to 1 mm in right chest leads V3R to V7R in the diagnosis of right ventricular infarction was investigated in a clinical and necropsy study of 43 consecutive patients who died in a coronary care unit. Thirty six patients had left ventricular myocardial infarction and in 27 the right ventricle was also affected. Seven patients had normal hearts. The specificity and positive predictive value of ST elevation in V3R were 81% and 77%, respectively. These increased to 100% when combined with ST elevation in one or more leads V4R-V7R. The diagnostic accuracy was poor for anterior infarcts (sensitivity less than or equal to 27%), but high for inferior/posterior infarcts (sensitivity greater than or equal to 64%) in which the specificity and positive predictive value reached 100% in V6R and V7R. Inferior/posterior infarction affecting the right ventricle can be diagnosed reliably by examination of electrocardiograms from right chest leads V6R and V7R.
Adult↗
Isolated necrotizing panarteritis of the gallbladder. Case report.
Two cases of isolated gallbladder involvement by necrotizing panarteritis histologically resembling classic polyarteritis nodosa are reported and the literature is reviewed. No reports suggest that isolated gallbladder involvement may evolve to systemic ('classic') polyarteritis nodosa. Finding of necrotizing panarteritis in the gallbladder without clinical evidence of systemic/multiorgan disease does not warrant extensive investigations.
Adult↗
Cardiac causes of death in hypertension.
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Cardiovascular Diseases↗
[Noise development in incubators].
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Adolescent↗
Comparative responses of radioattenuated Trypanosoma brucei and T. congolense in rats.
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Animals↗
The histology of myocardium in malignant hyperthermia: a preliminary report of 11 cases.
The preliminary results of a retrospective examination of the myocardium from 11 patients who responded to general anaesthesia with malignant hyperthermia are presented. Light-microscopical examination of the sections revealed no specific changes due to malignant hyperthermia. Contraction bands were demonstrated in 4 cases and it is concluded that the present investigation does not support the suggestion that a specific myofibrillar damage is responsbile for the arrhythmias seen in malignant hyperthermia.
Adult↗