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Biomedical subjects

F W Verheugt

Publications and source records attributed to F W Verheugt.

At least 145 records · Page 8Linked to original sources
PubMed1986

Effects of early intracoronary streptokinase on infarct size estimated from cumulative enzyme release and on enzyme release rate: a randomized trial of 533 patients with acute myocardial infarction.

The effects of early intracoronary streptokinase (SK) on enzymatic infarct size and rate of enzyme release were studied in a randomized multicenter trial. A total of 533 patients with acute myocardial infarction (AMI) were allocated to either the SK treatment group (n = 269) or the conventional (control) treatment group (n = 264). Enzymatic infarct size was represented by the cumulative quantity of alpha-hydroxybutyrate dehydrogenase (HBDH) released by the heart per liter of plasma in the first 72 hours. Rate of enzyme release was represented by the ratio of HBDH quantities released in 24 hours and 72 hours. On an "intention to treat" basis, the SK group had a smaller (by 30%; p = 0.0001) median enzymatic infarct size and a higher (by 35%; p = 0.0001) median rate of enzyme release than the control group. Limitation of infarct size was less apparent in patients treated with intracoronary SK only (25%) than in patients treated with intravenous plus intracoronary SK (34%). Compared to the control group, the enzyme release rate in patients treated with intracoronary SK only was slightly less (34%) than that in patients treated with intravenous plus intracoronary SK (38%). Patients with a patent infarct-related coronary artery at acute angiography had a median infarct size which was 55% (p = 0.0001) smaller than the median infarct size of the control group, and the median rate of enzyme release was 38% (p = 0.001) higher than the median release rate of the control group. Patients with successful recanalization during intracoronary SK infusion had a median infarct size which was 31% (p = 0.002) smaller than the median infarct size of the control group and a median rate of enzyme release which was 42% (p = 0.0001) higher than the median release rate of the control group. Patients with persistent coronary occlusion in spite of thrombolytic therapy had a median infarct size which was 11% (NS) higher than the median infarct size of the control group, although the median rate of enzyme release was still 23% (p = 0.02) higher than the median release rate of the control group. It is concluded that thrombolysis in the early phase of AMI limits infarct size and that intracoronary SK treatment itself accelerates the process of enzyme release from infarcted myocardium, independent of the angiographic result.

Clinical Trials as Topic↗
PubMed1986

Early thrombolysis in acute myocardial infarction: limitation of infarct size and improved survival.

The effect of thrombolysis in acute myocardial infarction on infarct size, left ventricular function, clinical course and patient survival was studied in a randomized trial comparing thrombolysis (269 patients) with conventional treatment (264 control patients). All 533 patients were admitted to the coronary care unit within 4 hours after the onset of symptoms related to the infarction. Baseline characteristics were similar in both groups. Informed consent was requested only of patients allocated to thrombolysis; no angiography was performed in 35. The infarct-related artery was patent in 65 patients and occluded in 169. Recanalization was achieved in 133 patients. The median time to angiographic documentation of vessel patency was 200 minutes after the onset of symptoms. The clinical course in the coronary care unit was more favorable after thrombolysis. Infarct size, estimated from myocardial enzyme release, was 30% lower after thrombolysis. In patients admitted within 1 hour after the onset of symptoms the reduction of infarct size was 51%, in those admitted between 1 and 2 hours it was 31% and in those admitted later than 2 hours it was 13%. Left ventricular function measured by radionuclide angiography before hospital discharge was better after thrombolysis (ejection fraction 48 +/- 15%) than in control patients (44 +/- 15%). Similar improvement was observed in patients with a first infarct only (thrombolysis 50 +/- 14%, control subjects 46 +/- 15%), in patients with anterior infarction (thrombolysis 44 +/- 16%, control subjects 35 +/- 14%) and in those with inferior infarction (thrombolysis 52 +/- 12%, control subjects 49 +/- 12%). Similar results were obtained by contrast angiography. Mortality was lower after thrombolysis. After 28 days 16 patients allocated to thrombolysis and 31 control patients had died. One year survival rates were 91 and 84%, respectively. On the other hand, nonfatal reinfarction occurred more frequently after thrombolysis (36 patients) than in control subjects (16 patients). Early thrombolysis by intracoronary streptokinase leads to a smaller infarct size estimated by enzyme release, preserves left ventricular function at the second week and leads to improved 1 year survival.

Aged↗
PubMed1986

Long term improvement in global left ventricular function after early thrombolytic treatment in acute myocardial infarction. Report of a randomised multicentre trial of intracoronary streptokinase in acute myocardial infarction.

The effect of reperfusion achieved by early intracoronary streptokinase in acute myocardial infarction on left ventricular function was studied in 533 patients enrolled in a prospective randomised multicentre study. Two hundred and sixty four patients were allocated to conventional treatment and 269 patients to thrombolysis. At the end of the procedure patency of the infarct related vessel was achieved in 198 (85%) of 234 patients in whom coronary angiography was performed. The median interval from onset of symptoms till the angiographic documentation of patency was 200 minutes. Data were analysed according to the original treatment allocation. Global left ventricular ejection fraction was determined by radionuclide angiography in 418 patients within two days of admission, in 361 patients after two weeks, and in 307 patients after three months. Global left ventricular function remained unchanged throughout the observation period in the control group, whereas it improved during the first two weeks in patients allocated to thrombolytic treatment. Improved function in these patients persisted up to three months after the infarction. Global left ventricular ejection fraction was significantly better in the thrombolysis group than in the control group at two days, two weeks, and at three months. In patients with anterior myocardial infarction the left ventricular ejection fraction was 9% better than in the control group at two weeks and at three months. In the patients with inferior myocardial infarction differences between the two treatment groups were smaller because of photon attenuation within the body. Angiographic evidence suggested that the improvement in function seen after thrombolysis is indeed associated with the patency of the infarct related artery.

Aged↗
PubMed1986

Prediction of spontaneous coronary reperfusion in myocardial infarction.

To investigate the possibility of predicting the occurrence of spontaneous coronary reperfusion in acute myocardial infarction we studied 91 patients in a randomized trial on the clinical efficacy of intracoronary streptokinase compared to conventional treatment. Of the 46 patients treated conventionally 40 had catheterization 6 weeks after the infarction. Spontaneous coronary reperfusion was found in 19 patients (48%). The time to peak CK-MB in these patients was considerably longer than in patients with streptokinase-induced coronary reperfusion and similar to the time in patients without spontaneous coronary reperfusion. Spontaneous coronary reperfusion was associated with a relative improvement of radionuclide ejection fraction from day 1 to day 14 after admission. There was no difference in the occurrence of ventricular arrhythmia or recurrent ischaemic events between the patients with and those without spontaneous coronary reperfusion. Thus, spontaneous coronary reperfusion is not uncommon in traditionally treated myocardial infarction, but its occurrence cannot be predicted by enzymatic or clinical parameters.

Clinical Trials as Topic↗
PubMed1986

Which patients benefit most from early thrombolytic therapy with intracoronary streptokinase?

The effect of thrombolysis in acute myocardial infarction on enzymatic infarct size, left ventricular function, and early mortality was studied in subsets of patients in a randomized trial. Early thrombolytic therapy with intracoronary streptokinase (152 patients) or with intracoronary streptokinase preceded by intravenous streptokinase (117 patients) was compared with conventional treatment (264 patients). All 533 patients were admitted to the coronary care unit within 4 hr after onset of symptoms indicative of acute myocardial infarction. Four hundred eighty-eight patients were eligible for this detailed analysis, and 245 of these were allocated to thrombolytic therapy and 243 to conventional treatment. Early angiographic examinations were performed in 212 patients allocated to thrombolytic therapy. Patency of the infarct-related artery was achieved in 181 patients (85%). Enzymatic infarct size, as measured from cumulative alpha-hydroxybutyrate dehydrogenase release, was smaller in patients allocated to thrombolytic therapy (median 760 vs 1170 U/liter in control patients, p = .0001). Left ventricular ejection fraction measured by radionuclide angiography before discharge from the hospital was higher after thrombolytic therapy (median 50% vs 43% in control patients, p = .0001). Three month mortality was lower in patients allocated to thrombolytic therapy (6% vs 14% in the control group, p = .006). With the use of multivariate regression analysis, infarct size limitation, improvement in left ventricular ejection fraction, and three month mortality were predicted by sum of the ST segment elevation, time from onset of symptoms to admission, and Killip class at admission. Thrombolysis was most effective in patients admitted within 2 hr after onset of symptoms and in patients with a sum of ST segment elevation of 1.2 mV or more. On the other hand, no beneficial effects of streptokinase on enzymatic infarct size, left ventricular function, or mortality were observed in the subset of patients with a sum of ST segment elevation of less than 1.2 mV who were admitted between 2 and 4 hr after onset of symptoms.

Cardiac Catheterization↗
PubMed1986

Effects of intracoronary thrombolysis on global left ventricular function assessed by an automated edge detection technique.

Three hundred and two patients with acute myocardial infarction were enrolled in a randomized multicenter trial to compare conventional treatment with attempted recanalization by intracoronary streptokinase. In a subgroup of patients, the effects of thrombolysis on left ventricular function were evaluated within 48 hr, at 2 wk, and at 3 mo after admission. Global left ventricular ejection fraction (LVEF) was obtained by radionuclide angiography and analyzed with an automatic detection program. Paired data were determined in 160 patients (control 78, thrombolysis 82) within 48 hr and at 2 wk, and in 143 patients (control 71, thrombolysis 72) at 48 hr, 2 wk, and 3 mo. It was shown that LVEF significantly improved in the thrombolysis group as compared with controls both at 2 wk (delta LVEF thrombolysis 3.9 +/- 7.9%, p less than 0.001 compared with delta LVEF control 0.6 +/- 9.7%, p = N.S.) and at 3 mo (delta LVEF thrombolysis 3.1 +/- 12.4%, p less than 0.05 compared with delta LVEF control 2.1 +/- 12.2%, p = N.S.). When patients were divided according to infarct site, however, significant improvement at 3 mo was only observed in the patients with anterior infarction (delta LVEF thrombolysis 5.5 +/- 13.1%, p less than 0.05 compared with delta LVEF control 3.3 +/- 10.4%, p = N.S.). It was shown that acute intervention with intracoronary streptokinase has a potentially favorable and lasting effect on left ventricular function in patients with anterior myocardial infarction. This improvement might be related to the rather rapid administration of thrombolytic therapy with a median time of approximately 4 hr after onset of symptoms.

Adult↗
PubMed1985

Improved survival after early thrombolysis in acute myocardial infarction. A randomised trial by the Interuniversity Cardiology Institute in The Netherlands.

Two strategies for treatment of acute myocardial infarction were compared in a randomised trial of 533 patients admitted within 4 h of the onset of symptoms. 264 patients were allocated to conventional treatment and 269 patients to a strategy aimed at rapid recanalisation of the occluded coronary artery. At first, intracoronary streptokinase (up to 250 000 U) was given immediately after angiography. In the last 117 patients intracoronary administration was preceded by intravenous streptokinase (500 000 U). No angiography was done in 35 patients allocated to thrombolytic therapy. Among the 234 patients who underwent angiography the infarct-related coronary artery was patent on admission or recanalised in 198 (85%). The median time between onset of symptoms and angiographic confirmation of a patent infarct-related artery was 200 min. Mortality was lower in patients randomised to thrombolysis than in controls at 28 days (16 v 31 patients) and at 8 months (23 v 42); 1-year survival was higher after thrombolysis (91%) than conventional treatment (84%). The clinical course in hospital was more favourable in patients allocated to thrombolysis, with a lower incidence of ventricular fibrillation (38 v 61), pericarditis (19 v 46), and cardiogenic shock (13 v 24), although they had a higher frequency of bleeding episodes (53 v 7). Non-fatal reinfarction was commoner after thrombolysis than after conventional therapy (36 V 16 patients). In both groups reinfarctions occurred predominantly in the same area as the initial infarct.

Aged↗
PubMed1985

Bleeding complications of intracoronary fibrinolytic therapy in acute myocardial infarction. Assessment of risk in a randomised trial.

The risk of bleeding associated with intracoronary infusion of streptokinase in acute myocardial infarction was determined in a randomised controlled trial containing 302 patients under the age of 70. Intracoronary streptokinase infusion was given to 152 patients and 150 patients were treated conventionally. Bleeding was seen in 24 (16%) patients in the streptokinase group and in two of the conventionally treated patients. Bleeding was most common (28%) in patients over the age of 60 years. The groin was the site of bleeding in all patients except one. In the first 48 hours after admission the haematocrit in streptokinase treated patients with manifest bleeding fell by 0.07 (0.04) (mean (SD)). The fall in haematocrit in the streptokinase treated patients without manifest bleeding was 0.05 (0.04) and in the conventionally treated patients it fell by 0.03 (0.04). Sixty six units of packed cells were transfused in the streptokinase group (50 units to those who bled); the control group required only 17 units. There were no deaths due to bleeding. The occurrence of bleeding and the fall in haematocrit in the streptokinase group correlated with the occurrence of systemic fibrinolysis but not with the dose of streptokinase given. Thus, in about 15% of patients treatment with intracoronary streptokinase resulted in significant non-fatal bleeding from the femoral puncture site that required substantial transfusion support. Furthermore, there was a significant drop in haematocrit in patients without manifest bleeding. These results emphasise the need for more specific fibrinolytic agents.

Clinical Trials as Topic↗
PubMed1984

Left ventricular platelet deposition after acute myocardial infarction. An attempt at quantification using blood pool subtracted indium-111 platelet scintigraphy.

Since indium-111 platelet scintigraphy for the detection of left ventricular thrombosis often shows considerable non-specific blood pool activity a subtraction method using simultaneous technetium-99m blood pool scintigraphy was undertaken in 11 subjects with well documented remote myocardial infarction, who served as positive or negative controls, and in 18 consecutive patients with acute myocardial infarction. The results were compared with those of cross sectional echocardiography. Thirteen patients had transmural myocardial infarction and the calculated count per pixel in the left ventricle of the subtracted indium-111 platelet scintigram was (mean (SD)) 0.28(0.35), but five patients with subendocardial myocardial infarction had a mean count of 0.04(0.06). In seven patients with transmural myocardial infarction (two anterior and five inferior) left ventricular thrombosis was detected by indium-111 platelet scintigraphy but in only one of these by cross sectional echocardiography. None of the patients with subendocardial myocardial infarction had left ventricular thrombosis. Subtracted left ventricular counts correlated well with the visual results. It is concluded that left ventricular platelet sequestration after acute myocardial infarction may be quantified and precisely located and that quantitative longitudinal studies of the natural history and drug intervention are now possible.

Adult↗
PubMed1983

Intracoronary platelet release in patients with and without coronary artery disease.

Intracoronary platelet release of beta-thromboglobulin (BTG) was measured in 18 patients with a history of chest pain by analysis of aortic and coronary sinus blood samples in rest and during atrial pacing. Eleven proved to have coronary artery disease, while seven had normal coronary arteriograms and served as controls. In both groups no statistically significant transmyocardial gradient of platelet and plasma BTG content was observed under basal conditions, although the aortic plasma BTG levels in the patients (60.4 +/- 4.1 ng/ml) were significantly (p less than 0.05) higher than in the controls (47.5 +/- 2.6 ng/ml). However, also during atrial pacing no significant gradient could be demonstrated in the patients nor in the controls. It is concluded, that in stable coronary artery disease measurable intracoronary platelet release does not occur in rest nor atrial pacing and, therefore, does not seem to contribute to the development of exercise-induced myocardial ischaemia.

Blood Platelets↗
PubMed1982

Alternating atrial electromechanical dissociation as contributing factor for pulsus alternans.

Ten patients with mechanical pulsus alternans were studied by echocardiography and mechanocardiography. All had been or were in congestive heart failure. An atrial mechanism for pulsus alternans could be identified in two patients: one with primary congestive cardiomyopathy and one after aortic valve replacement for calcific aortic stenosis. Each strong systole was preceded by an "a" wave, while each weak systole was not. This was documented on both the apexcardiogram and the M-mode echocardiogram. Since both patients were in normal sinus rhythm with regular PP intervals, it was concluded that alternating atrial electromechanical dissociation was either the underlying mechanism or contributed to the pulsus alternans. Thus, alternating atrial electromechanical dissociation exists and may cause pulsus alternans. Pulsus alternans is not necessarily the result of left ventricular myocardial dysfunction alone.

Adult↗
PubMed1982

Effect of nicotine on production of prostacyclin in human umbilical artery.

The influence of nicotine on the production of prostacyclin was studied in umbilical arteries from newborn infants of mothers who were smokers and those who were non-smokers. Thirteen umbilical cords were obtained from the non-smokers and 10 from the smokers. After their ability to produce prostacyclin was shown, the arteries were perfused during a 20 minute period with nicotine 10-7 mol in Krebs-Henseleit buffer and then again during 20 minutes with pure buffer. Nicotine led to a decline in prostacyclin production in all but one artery. In five of 12 arteries from mothers who did not smoke the production recovered during buffer reperfusion, while in nine of 10 arteries from mothers who smoked, prostacyclin production declined to lower levels and did not increase during 20 minutes buffer reperfusion. It is concluded that nicotine has a direct depressive effect on the prostacyclin production in the vascular wall, which in turn may lead to increased platelet aggregation and thus be a precursor of vascular lesions.

Adult↗