PubMed Health⌕ Search

Biomedical subjects

W T Hermens

Publications and source records attributed to W T Hermens.

At least 55 records · Page 3Linked to original sources
PubMed1997

Adenoviral vector-mediated gene transfer and neurotransplantation: possibilities and limitations in grafting of the fetal rat suprachiasmatic nucleus.

Several studies have reported on the use of primary neural cells transduced by adenoviral vectors as donor cells in neurotransplantation. In the present investigation, we examined whether adenoviral vector-mediated gene transfer could be used to introduce and express a foreign gene in solid neural transplants of fetal suprachiasmatic nucleus (SCN) tissue. A recombinant adenoviral vector containing the reporter gene LacZ encoding for beta-galactosidase (Ad-LacZ) was used in order to establish the optimal procedure for ex vivo gene transfer. Expression of beta-galactosidase was dependent on the duration of the infection and on the vector concentration. Infection for a short period (< 4 h) with a high concentration of Ad-LacZ (3.4 x 10(9) pfu/ml), or for 18 h with a lower vector concentration (2 x 10(8) pfu/ml), resulted in expression of beta-galactosidase in a large number of neurons and glial cells up to 21 days in vitro. When infected fetal SCN tissue was implanted in the third ventricle of adult Wistar rats, expression was high after 8 days. After 21 days, the number of beta-galactosidase expressing cells had clearly declined, but expression remained present for at least 70 days. The method described in this paper might be applicable to introduce trophic factor genes in SCN grafts in order to support graft survival and to stimulate neurite outgrowth.

Adenoviridae↗
PubMed1997

A role for secretory phospholipase A2 and C-reactive protein in the removal of injured cells.

The acute phase response is initiated in response to infection or physical trauma and is characterized by an increase in the levels of some plasma proteins. Here, Erik Hack and colleagues suggest that the combined actions of two of these acute phase proteins, secretory phospholipase A2 and C-reactive protein, may serve to promote phagocytosis of injured cells and tissue debris, thereby enhancing inflammation and tissue damage.

Acute-Phase Reaction↗
PubMed1997

Dye extravasation and the nature of background fluorescence in sodium fluorescein angiography.

PURPOSE: To obtain better insight into the process of dye extravasation in the human choroid during sodium fluorescein angiography of the ocular fundus. METHODS: Sodium fluorescein angiography using a scanning laser ophthalmoscope was performed on the right eye of five healthy volunteers. The dose of sodium fluorescein was chosen to avoid quenching in the ocular vessels. The time-intensity curve of background fluorescence was measured and its shape compared with that of the time-intensity curve of a retinal artery, representing an intravascular compartment. Significant dye extravasation is expected to cause a marked change in shape of the time-intensity curve of background fluorescence as compared with the intravascular time-intensity curve due to long washout of dye from the interstitial space of the choroid. RESULTS: In all five subjects, the time-intensity curve of background fluorescence and the retinal artery proved to be quite similar in shape until several seconds after peak intensity of the first bolus passage. CONCLUSION: Background fluorescence originates mainly from intravascular compartments during the early phase of the sodium fluorescein angiogram.

Adult↗
PubMed1997

Estimation of myocardial infarct size from plasma myoglobin or fatty acid-binding protein. Influence of renal function.

Myoglobin (M(r) 18,000) and fatty acid-binding protein (M(r) 15,000), are low molecular mass cytoplasmic proteins that are considered useful biochemical markers for early detection or exclusion of acute myocardial infarction, and also for early estimation of infarct size. As each of these proteins shows renal clearance, we studied the influence of renal function on the estimation of infarct size from their plasma concentration curves. For this, infarct size estimated from plasma myoglobin or fatty acid-binding protein release curves was compared with that estimated with the established infarct size markers hydroxybutyrate dehydrogenase and creatine kinase, which are not influenced by changes in renal function. The discordance between infarct size estimates was related to renal function. Creatine kinase (EC 2.7.3.2), hydroxybutyrate dehydrogenase (EC 1.1.1.27), myoglobin, fatty acid-binding protein and creatinine were assayed serially in plasma samples obtained frequently and for at least 72 hours after the start of thrombolytic therapy in 20 patients with acute myocardial infarction. Cumulative release of the different cardiac markers was calculated by using a two-compartment model for circulating proteins. Mean tissue contents of 156 U/g for hydroxybutyrate dehydrogenase, 2163 U/g for creatine kinase, 2.79 mg/g for myoglobin and 0.57 mg/g wet weight for fatty acid-binding protein, were used to express infarct size in gram-equivalents of healthy myocardium per litre of plasma (g-eq/l). Mean plasma creatinine was obtained by averaging the creatinine concentrations measured in all plasma samples taken during the first 24 hours after acute myocardial infarction. A relation was found between the mean plasma creatinine concentration during the first 24 hours after acute myocardial infarction and the discordance between infarct size estimated from cumulative hydroxybutyrate dehydrogenase release, compared to infarct size estimated from cumulative myoglobin or fatty acid-binding protein release. For patients with mean plasma creatinine concentrations within the reference interval for creatinine (group 1, n = 15) a good agreement was found between infarct size estimated from myoglobin or fatty acid-binding protein plasma curves and that estimated with either hydroxybutyrate dehydrogenase or creatine kinase. However, for patients with a mean creatinine concentration above the upper reference limit (group 2, n = 5), infarct size calculated from plasma myoglobin or fatty acid-binding protein release curves was markedly overestimated, especially for larger infarcts. Estimation of infarct size from serial plasma myoglobin or fatty acid-binding protein concentrations is possible in the first 24 hours after the onset of symptoms, but only in patients with normal renal function, as estimated from plasma creatinine concentrations.

Adult↗
PubMed1997

Cumulative troponin T release after acute myocardial infarction. Influence of reperfusion.

UNLABELLED: For troponin T a characteristic biphasic change in the plasma time-concentration curve has been described, especially in patients with early reperfusion after thrombolytic therapy. As troponin T is bound to myofibrillar structures, treatment strategy or treatment outcome could influence the cumulative plasma release of this protein in a different way compared to the cumulative release of free cytoplasmic cardiac enzymes. The present study is the first study comparing the total quantity of troponin T released by the heart during the first 168 hours after acute myocardial infarction, both in patients treated with thrombolytic therapy (n = 16) and in patients not treated with thrombolytic therapy (n = 7). On the basis of clinical symptoms and coronary arteriogram within 24 hours, the patients treated with thrombolytic therapy were divided into two groups, reperfused (n = 9) and non-reperfused (n = 7). In the patients not treated with thrombolytic therapy, absence of spontaneous early reperfusion was judged only from clinical symptoms. Cumulative troponin T release into plasma was compared to the cumulative release of the cytoplasmic cardiac enzymes creatine kinase (EC 2.7.3.2) and hydroxybutyrate dehydrogenase (EC 1.1.1.27). Cumulative release, i. e., infarct size, was calculated using a two-compartment model for circulating proteins. Mean tissue contents, per gram wet weight, of 156 U/g for hydroxybutyrate dehydrogenase, 2.163 U/g for creatine kinase and 234 microg/g for troponin T, were used to express infarct size in gram-equivalents of healthy myocardium per litre plasma (g-eq/l). Release rates were represented by the ratio of cumulative quantities released in 10 hours and 72 hours for creatine kinase and hydroxybutyrate dehydrogenase and in 10 hours and 168 hours for troponin T. CONCLUSIONS: - Plasma time-concentration curves and release rates of troponin T in patients treated with thrombolytic therapy showing reperfusion differ significantly from those of patients not treated with thrombolytic therapy, showing no reperfusion. - Creatine kinase and hydroxybutyrate dehydrogenase release is completed within 72-100 hours in all patients, whereas troponin T release still continues after 168 hours. - Cumulative troponin T release at 168 hours is only a fraction (around 8%) of cumulative cytoplasmic enzyme release and the percentage released is not influenced by the treatment strategy or outcome, i. e., vessel patency. - Although troponin T release is only a fraction of the cumulative enzyme release (infarct size) there is a highly significant correlation between both, independent of the treatment strategy or treatment outcome.

Aged↗
PubMed1996

Efficient adenoviral vector-directed expression of a foreign gene to neurons and sustentacular cells in the mouse olfactory neuroepithelium.

Replication deficient recombinant adenoviral vectors are efficient gene transfer agents for postmitotic cells, including neurons and glial cells. In this paper we have examined the effectiveness of adenoviral vector-mediated gene transfer to the olfactory epithelium of adult mice. We show that Ad-LacZ, a prototype first generation adenoviral vector containing an expression cassette for the reporter gene LacZ, directs transgene expression to mature and immature olfactory neurons and to sustentacular cells. The technique to apply the vector to the nasal cavity and the amount of viral vector per mouse are important variables that determine the success of viral vector-mediated gene transfer to the mouse olfactory neuroepithelium. Slow infusion of the viral vector solution in fully anaesthetized mice yields the best result in terms of the number of epithelial cells transduced. Infection of the olfactory neuroepithelium with a moderate amount of viral vector (10(9) plaque-forming units (PFU)) results in transgene expression in many cells throughout the epithelium for 8-12 days, followed by a decline in transduced cells at 25 days postinstillation of the virus This decrement in transgene expression is consistent with the natural turnover process that occurs in the epithelium throughout adulthood. At high viral loads (1.3 x 10(10) PFU) extinction of transgene expression occurs as early as 8 days postinjection and is accompanied by epithelial degeneration indicating that the vector dose used should be carefully chosen. Taken together, the current observations demonstrate that adenoviral vectors are effective tools to genetically modify the adult mouse olfactory neuroepithelium in vivo.

Adenoviruses, Human↗
PubMed1996

Critical micelle concentrations and stirring are rate limiting in the loss of lipid mass during membrane degradation by phospholipase A2.

In phospholipid membranes attacked by phospholipase A(2) (PLA(2)), accumulation of degradation products influences the binding affinity as well as the catalytic activity of PLA(2). Such accumulation in its turn depends on the rate of membrane degradation and the efflux of degradation products from the membrane, the latter being influenced by the stirring conditions in the system. This complicated process was investigated with a new ellipsometric technique for in situ measurement of membrane mass in a well-defined flow system. Planar phospholipid bilayers were formed on rotating silicon discs in buffer solution. After the addition of 0.05-100 ng/ml of PLA(2) (from Naja mocambique mocambique) to the buffer, mass desorption could be measured with a precision of 3-5 ng/cm(2), that is, about 1% of the surface mass of a single bilayer. Using radiolabeled phospholipids and thin-layer chromatography, it was verified that only the degradation products desorb from the membrane, which was confirmed by the desorption of mixtures of phospholipids, lysophospholipids, and fatty acids. The rotating disc allows the exact calculation of the mass transfer constant for transport-limited exchange of lipid between fluid and disc surface, as a function of rotation rate. By using the mass transfer constant, the critical micelle concentrations, and the mole fractions of products, desorption kinetics could be fully described. The amount of degraded phospholipid could be continuously monitored as the sum of the product mass still present in the membrane, as inferred from the desorption rate, and the mass already lost from the surface. It is concluded that ellipsometry is a suitable tool for studying the effects of PLA(2) on membranes.

Adsorption↗
PubMed1996

Differential effects of tissue plasminogen activator and streptokinase on infarct size and on rate of enzyme release: influence of early infarct related artery patency. The GUSTO Enzyme Substudy.

BACKGROUND: The recent international GUSTO trial of 41,021 patients with acute myocardial infarction demonstrated improved 90-min infarct related artery patency as well as reduced mortality in patients treated with an accelerated regimen of tissue plasminogen activator, compared to patients treated with streptokinase. A regimen combining tissue plasminogen activator and streptokinase yielded intermediate results. The present study investigated the effects of treatment on infarct size and enzyme release kinetics in a subgroup of these patients. METHODS: A total of 553 patients from 15 hospitals were enrolled in the study. Four thrombolytic strategies were compared: streptokinase with subcutaneous heparin, streptokinase with intravenous (i.v.) heparin, tissue plasminogen activator with i.v. heparin, and streptokinase plus tissue plasminogen activator with i.v. heparin. The activity of alpha-hydroxybutyrate dehydrogenase (HBDH) in plasma was centrally analysed and infarct size was defined as cumulative HBDH release per litre of plasma within 72 h of the first symptoms (Q(72)). Patency of the infarct-related vessel was determined by angiography in 159 patients, 90 min after treatment. RESULTS: Infarct size was 3.72 g-eq.1(-1) in patients with adequate coronary perfusion (TIMI-3) at the 90 min angiogram and larger in patients with TIMI-2 (4.35 g-eq.1(-1) or TIMI 0-1 (5.07 g-eq.1(-1) flow (P = 0.024). In this subset of the GUSTO angiographic study, early coronary patency rates (TIMI 2 + 3) were similar in the two streptokinase groups (53 and 46%). Higher, but similar, patency rates were observed in the tissue plasminogen activator and combination therapy groups (87 and 90%). Median infarct size for the four treatment groups, expressed in gram-equivalents (g-eq) of myocardium, was 4.4, 4.5, 3.9 and 3.9 g-eq per litre of plasma (P = 0.04 for streptokinase vs tissue plasminogen activator). Six hours after the first symptoms, respectively 5.3, 6.6, 14.0 and 13.6% of total HBDH release was complete (P < 0.0001 for streptokinase vs tissue plasminogen activator). CONCLUSIONS: Rapid and complete coronary reperfusion salvages myocardial tissue, resulting in limitation of infarct size and accelerated release of proteins from the myocardium. Treatment with tissue plasminogen activator, resulting in earlier reperfusion was more effective in reducing infarct size than the streptokinase regimens, which contributes to the differences in survival between treatment groups in the GUSTO trial.

Humans↗
PubMed1996

Cardiac troponin T release into plasma after acute myocardial infarction: only fractional recovery compared with enzymes.

After acute myocardial infarction (AMI) cardiac enzymes and proteins are released into plasma and are used as biochemical markers of cardiac muscle injury. We studied the completeness of the release of troponin T, a cardiac protein that is largely bound to myofibrillar structures and compared it with the release of cytoplasmic cardiac enzymes in 22 patients with AMI, who were treated with thrombolytic therapy. Creatine kinase (CK; EC 2.7.3.2), hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LDH; EC 1.1.1.27) and troponin T were assayed serially in plasma samples obtained frequently and for at least 168 h after the start of thrombolytic therapy. Cumulative release of enzymes and troponin T in plasma were calculated by using a two-compartment model for circulating proteins. In order to express the cumulative plasma releases in gram equivalent (g-eq) healthy myocardium per litre plasma (infarct size), we determined HBDH, LDH and total troponin T contents per gram net weight of tissue in 17 human hearts obtained post-mortem from patients who died from non-cardiac causes. Mean (SD) tissue contents per gram wet weight of, respectively, 156 +/- 25 U/g, 385 +/- 59 U/g and 234 +/- 65 micrograms/g were found. For the cardiac enzymes CK, HBDH and LDH the mean (SEM, n = 22) total release over 72 h, was, respectively, 5.9 +/- 1.5, 5.9 +/- 1.6 and 6.1 +/- 1.7 g-eq/L. There was no further increase after 72 h and the differences between enzymes were not significant. The mean (SEM) cumulative troponin T release, expressed in gram equivalents of myocardium per litre of plasma was only 0.30 +/- 0.09 g-eq/L after 72 h and 0.51 +/- 0.61 g-eq/L after 168 h. After 72 h total recovery of troponin T in g-eq/L was only 5% and after 168 h only 8.5% of the total recovery of cytoplasmic cardiac enzymes after 72 h. Cumulative troponin T release after 72 h and after 168 h correlates well with infarct size, estimated from cumulative cytoplasmic enzyme release. However, quantification of infarct size should preferably be performed from plasma release curves of cytoplasmic cardiac enzymes or proteins in order to prevent underestimation of infarct size, caused by incomplete release of the non-cytoplasmic proteins.

Adult↗
PubMed1995

Discrimination between myocardial and skeletal muscle injury by assessment of the plasma ratio of myoglobin over fatty acid-binding protein.

BACKGROUND: Myoglobin and fatty acid-binding protein (FABP) each are useful as early biochemical markers of muscle injury. We studied whether the ratio of myoglobin over FABP in plasma can be used to distinguish myocardial from skeletal muscle injury. METHODS AND RESULTS: Myoglobin and FABP were assayed immunochemically in tissue samples of human heart and skeletal muscle and in serial plasma samples from 22 patients with acute myocardial infarction (AMI), from 9 patients undergoing aortic surgery (causing injury of skeletal muscles), and from 10 patients undergoing cardiac surgery. In human heart tissue, the myoglobin/FABP ratio was 4.5 and in skeletal muscles varied from 21 to 73. After AMI, the plasma concentrations of both proteins were elevated between approximately 1 and 15 to 20 hours after the onset of symptoms. In this period, the myoglobin/FABP ratio was constant both in subgroups of patients receiving and those not receiving thrombolytics and amounted to 5.3 +/- 1.2 (SD). In serum from aortic surgery patients, both proteins were elevated between 6 and 24 hours after surgery; the myoglobin/FABP ratio was 45 +/- 22 (SD), which is significantly different from plasma values in AMI patients (P < .001). In patients with cardiac surgery, the ratio increased from 11.3 +/- 4.7 to 32.1 +/- 13.6 (SD) during 24 hours after surgery, indicating more rapid release of protein from injured myocardium than from skeletal muscles. CONCLUSIONS: The ratio of the concentrations of myoglobin over FABP in plasma from patients with muscle injury reflects the ratio found in the affected tissue. Since this ratio is different between heart (4.5) and skeletal muscle (20 to 70), its assessment in plasma allows the discrimination between myocardial and skeletal muscle injury in humans.

Aged↗
PubMed1995

Production of thrombin as a probe for mixing of phospholipids in membranes on solid supports.

Phospholipid-covered solid supports have been used successfully as model membranes in studies on blood coagulation and other research fields. In order to produce such membranes, simple exposure of the support to suspensions of phospholipid vesicles was recently introduced, but questions have remained about the process of vesicle adherence to the surface and the physico-chemical properties of the resulting membranes. Using a new technique, mixing of phospholipids in such membranes was demonstrated. A rotating, hydrophilic, silicon disc was exposed in a two-step procedure to vesicles prepared from mixtures of dioleoylphosphatidylserine (DOPS) and dioleoylphosphatidylcholine (DOPC). Factor Xa, factor Va and prothrombin were added and the transport-limited production rate of thrombin was measured. For low surface coverage with 40% DOPS/60% DOPC, a much higher conversion rate was found if, prior to addition of coagulation factors, excess DOPC vesicles were added to fill up vacant surface area. It is concluded that DOPS is spread over the entire surface and that confluent bilayers are formed. The presented technique may also be used to measure lateral diffusion constants.

Diffusion↗
PubMed1995

Annexin V perturbs or stabilises phospholipid membranes in a calcium-dependent manner.

The potency of annexin V to transport Ca2+ ions across phospholipid membranes was investigated, using large unilamellar phospholipid vesicles loaded with the Ca2+ indicator fura-2. It was demonstrated that annexin V leaves the vesicle membranes intact when added in the presence of 1 mM Ca2+. However, if the vesicles were first incubated with annexin V in the absence of Ca2+, subsequent addition of Ca2+ produced a fluorescence signal due to binding of Ca2+ to fura-2. Centrifugation of the vesicle suspension immediately thereafter showed that this signal originated from the supernatant and not from the sedimented vesicles. Our results show that annexin V causes loss of vesicle integrity in the absence of Ca2+, and leakage of trapped fura-2, rather than inward Ca2+ transport. Bovine serum albumin or Ca2+ concentrations higher than 2.5 mM also caused such fura-2 leakage. Apparently, calcium-dependent binding of annexin V to the membrane prevents aspecific membrane damage caused by this protein.

Annexin A5↗
PubMed1994

Expression of the growth-associated protein B-50/GAP43 via a defective herpes-simplex virus vector results in profound morphological changes in non-neuronal cells.

This study describes the creation and application of a defective herpes simplex viral (HSV) vector for B-50/GAP-43, a neural growth-associated phosphoprotein. We demonstrate abundant expression of B-50/GAP-43 in cultured non-neuronal cells (African green monkey kidney cells [vero cells] and Rabbit skin cells) via this HSV vector. When B-50/GAP-43 was expressed in non-neuronal cells major morphological changes occurred that included extensive membrane ruffling, the formation of filopodia and long thin extensions reminiscent of neurites. These extensions often terminated in growth cone-like structures. Quantitation of these morphological changes at different times following infection demonstrates that the surface area of the B-50/GAP-43-expressing cells started to increase between 6 and 10 h post-infection. At 72 h, B-50/GAP-43-positive cells were 3.0 times larger in size and one third of the cells expressed long processes with a mean length of 165 +/- 14.5 microns. Ultrastructural studies of cells 48 h after infection revealed that B-50/GAP-43 is predominantly localized at the plasma membrane of the elaborated processes. Some immunoreactivity was associated with vesicular structures that appear to be in-transit in the processes. These observations suggest that B-50/GAP-43 acts at the plasmamembrane to induce a neuron-like morphology in non-neuronal cells persisting for several days in culture. In the future the defective viral vector will enable gene transfer to express B-50/GAP-43 in neurons in vivo in order to study its involvement in regenerative sprouting and neuroplasticity.

Animals↗
PubMed1994

Fatty-acid-binding protein as a plasma marker for the estimation of myocardial infarct size in humans.

BACKGROUND: There are substantial amounts of cytoplasmic heart-type fatty-acid-binding protein (FABP) (15 kDa) in myocardial tissue. The rapid release of FABP into plasma during ischaemia indicates the possibility of using this protein as a biochemical marker for ischaemic myocardial injury. OBJECTIVE: To study the completeness of the release of FABP from damaged tissue in patients with acute myocardial infarction (AMI) and the suitability of serial plasma FABP concentrations for estimation of myocardial infarct size. METHODS: Immunochemically assayed FABP and enzymatically assayed creatine kinase isoenzyme MB (CK-MB) and alpha-hydroxybutyrate dehydrogenase (HBDH) were determined serially in plasma samples from 49 patients with AMI who had been treated with thrombolytic agents within six hours after the onset of AMI. Previously validated circulatory models and a value of 2.6 h-1 for the fractional clearance rate of FABP from plasma were used to calculate cumulative protein release into plasma. RESULTS: Release of FABP was completed earlier (24-36 h) after AMI than that of CK-MB (50-70 h) and that of HBDH (> 70 h). However, infarct size estimated from the cumulative release of the proteins and expressed as gram equivalents of healthy myocardium per litre of plasma yielded a comparable value of 4-6 for both FABP and the two enzymes. CONCLUSION: The data indicate that FABP released from the heart after AMI is quantitatively recovered in plasma and that FABP is a useful biochemical plasma marker for the estimation of myocardial infarct size in humans.

Adult↗
PubMed1994

Limitation of infarct size and preservation of left ventricular function after primary coronary angioplasty compared with intravenous streptokinase in acute myocardial infarction.

BACKGROUND: Early and effective flow through the infarct-related vessel is probably of paramount importance for limitation of infarct size and preservation of left ventricular function in patients with acute myocardial infarction. Primary coronary angioplasty may offer advantages in these respects compared with thrombolytic therapy. The purpose of the present study was to assess the effects on estimated enzymatic infarct size and left ventricular function in patients with acute myocardial infarction randomly assigned to undergo primary angioplasty or to receive intravenous streptokinase. METHODS AND RESULTS: We evaluated 301 patients with signs of acute myocardial infarction and without contraindications for thrombolysis who presented within 6 hours after onset of symptoms or between 6 and 24 hours if there was evidence of ongoing ischemia. One hundred fifty-two patients were randomly assigned to undergo primary angioplasty, and 149 patients were assigned to receive treatment with streptokinase (1.5 million U i.v.). Infarct size was estimated from enzyme release. Global left ventricular ejection fraction and regional wall motion, if possible in combination with exercise testing, were evaluated by radionuclide ventriculography before discharge. Thrombolysis in Myocardial Infarction (TIMI) flow grade 3 through the infarct-related vessel within 120 minutes after admission was achieved in 92% of all patients assigned to receive primary angioplasty therapy. Myocardial infarct size was 23% smaller in the angioplasty group compared with patients assigned to receive streptokinase (1003 +/- 784 versus 1310 +/- 1198 U/L, P = .012). Global left ventricular ejection fraction (50 +/- 9% versus 45 +/- 11%, P < .001) and regional wall motion in the infarct-related zones (42 +/- 14% versus 34 +/- 13%, P < .001) were better in the angioplasty group, which could mainly be contributed to myocardial salvage in the infarct-related areas. The observed differences were more pronounced in patients with an anterior wall myocardial infarction, although patients with a nonanterior infarct location also showed a beneficial effect of primary coronary angioplasty on left ventricular function compared with streptokinase therapy. Furthermore, the observed differences appeared to be more pronounced in patients presenting relatively early (within 2 hours) after onset of symptoms. CONCLUSIONS: In patients with acute myocardial infarction, primary angioplasty results in a smaller infarct size and a better preserved myocardial function compared with patients randomized to receive treatment with intravenous streptokinase. This is probably due to early and optimal blood flow through the infarct-related vessel, as can be accomplished in a very high percentage of patients undergoing primary coronary angioplasty.

Angioplasty, Balloon, Coronary↗