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Biomedical subjects

J Vanhaecke

Publications and source records attributed to J Vanhaecke.

At least 73 records · Page 4Linked to original sources
PubMed1989

Fatal aortic rupture: an unusual complication of percutaneous balloon valvuloplasty for acquired valvular aortic stenosis.

A case report complicated by a perforation of the ascending aorta during percutaneous balloon valvuloplasty for acquired aortic stenosis in a bicuspid aortic valve is presented. The clinical and pathological findings are discussed. It is suggested that in patients with hard calcified valve cusps and calcifications of the aortic annulus balloon sizes exceeding the aortic diameter should be avoided.

Aged↗
PubMed1989

Coronary reperfusion by thrombolysis and early beta-adrenergic blockade in acute experimental myocardial infarction.

The effects of beta-adrenergic blockade, thrombolysis and their combination on infarct size and left ventricular function were investigated in a canine model of thrombotic occlusion of the left anterior descending coronary artery. Metoprolol was administered intravenously (0.5 mg/kg) over 10 min, starting 15 min after occlusion. Recombinant human tissue-type plasminogen activator (rt-PA) was given intravenously 1 h after occlusion for clot lysis. Anatomic infarct size was measured as a percent of perfusion area and ventricular mass. Left ventricular function was assessed by ejection fraction and the centerline method. Groups 1, 3, 5 and 7 were evaluated after 24 h and received, respectively, metoprolol plus rt-PA, rt-PA, metoprolol and no treatment; groups 2, 4, 6 and 8 were studied after 1 week and treated, respectively, as groups 1, 3, 5 and 7. Metoprolol did not influence infarct size and global or regional ventricular function after 24 h and 1 week. Thrombolysis reduced infarct size from 69.5 +/- 3.4% (24 h) and 76.6 +/- 1.8% (1 week) in the control group to, respectively, 44.1 +/- 11.6% and 39.5 +/- 10.5% (p greater than 0.05), did not influence left ventricular function after 24 h and was accompanied after 1 week by a definite recovery of global and regional left ventricular function when compared with findings in control dogs. Metoprolol plus rt-PA further reduced infarct size (percent perfusion area) to 20.4 +/- 3.7% and 19.9 +/- 8.1% after 24 h and 1 week, respectively (p = NS versus rt-PA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Limitation of experimental infarct size by drugs.

Testing drugs on their efficacy in limiting infarct size is difficult in the experimental setting because of the considerable variation in the sizes of infarcts produced in control animals, mainly in dogs. This variation in infarct size in the canine model is theoretically related to variations in the size of the ischemic bed or area at risk, in pre-existing collateral blood flow, and in myocardial metabolic demand. In this study, we identified the determinants of infarct size after different periods of coronary artery occlusion in unconscious dogs and constructed a mathematical model based on these determinants using stepwise logistic regression analysis. Eighty-nine percent of the variability in infarct size is accounted for by variations in the size of the ischemic bed and coronary collateral blood flow. Using this model, we were able to predict infarct size and to make valid comparisons between treated and control groups.

Animals↗
PubMed1988

An unusual case of guide wire fracture during percutaneous transluminal coronary angioplasty.

We report a case of guide wire fracture during percutaneous transluminal coronary angioplasty, using one of the newer catheter systems. The broken free end of the guide wire remained within the coronary tree, and surgical removal was necessary. Entrapment and overcoiling of the guide wire can cause fracture; in our case excessive bending in a tortuous coronary tree resulted in this unusual complication. An excessive tensile load to the guide wire may result from anatomical peculiarities and can cause wire fracture.

Angioplasty, Balloon↗
PubMed1988

Histology of the postischaemic myocardium and its relation to left ventricular function.

The relation between the histology of the myocardium and left ventricular function was studied in 23 dogs submitted to 90 min of coronary artery occlusion followed by reperfusion for up to 1 week. It was shown that 32% of the perfusion area of the occluded coronary artery was irreversibly damaged. There was, however, no significant correlation between the decrease in left ventricular function (ejection fraction assessed by angiography) and the extent of myocardial necrosis. Upon reperfusion, salvage of 68% of the perfusion area of the occluded vessel was obtained. Viability of the myocardium in this area was demonstrated by electron microscopy. However, postischaemic regional function was completely lost in the first 24 h, in spite of this considerable amount of viable tissue. Nevertheless, regional function recovered after 1 week of reperfusion, which suggests a stunned myocardium in the early postischaemic phase. These results show that histological examination of postischaemic tissue has prognostic value in terms of recovery of function, but a direct correlation between structure and function does not exist in the early reperfusion phase.

Actin Cytoskeleton↗
PubMed1988

Long term spontaneous evolution of left ventricular function after experimental acute coronary occlusion.

In a canine model of acute occlusion of the left anterior descending artery (LAD), left ventriculography was performed before and immediately after occlusion and also one and three weeks later. Regional left ventricular function was evaluated by the centreline method. Global and regional left ventricular function were significantly depressed immediately after occlusion and showed no significant recovery after one and three weeks, except for a decrease in the paradoxical motion of the LAD territory, which was probably due to stiffening of the infarct area.

Angiocardiography↗
PubMed1988

[Randomized double-blind study comparing tissue-type plasminogen activator with placebo in acute myocardial infarct].

In a double-blind randomised trial 129 patients with first myocardial infarction of less than 6 h duration were allocated to treatment with human recombinant tissue-type plasminogen activator (rt-PA) given intravenously over 90 min, or to placebo infusion. Coronary angiography at the end of this infusion showed that the infarct-related vessel was patent in 61% of 62 assessable coronary angiograms in the rt-PA-treated group compared with 21% in the control group. Treatment with rt-PA was not accompanied by any major complications. In the rt-PA group the circulating fibrinogen level at the end of the catheterisation was 52 +/- 29% (mean +/- SD) of the starting value.

Adult↗
PubMed1988

Intravenous streptokinase during acute myocardial infarction. A prospective open study.

To evaluate the efficacy of intravenous streptokinase in acute myocardial infarction (AMI) 108 patients received a high-dose (1.5 million units), short-term infusion (60 minutes) within 6 hours after onset of symptoms, followed by anticoagulation. Before discharge a submaximal exercise test and a coronary arteriography were performed in 100 surviving patients. Sixty-seven patients had a patent infarct-related vessel. Clinical reocclusion occurred in 21 patients. Left ventricular function was slightly, but not significantly, better in patients with patent infarct-related vessels: ejection fraction 59.5 +/- 13% versus 57.4 +/- 13%. Additional procedures were performed in 20 patients: percutaneous transluminal coronary angioplasty (PTCA) in 8 and coronary artery bypass surgery (CABG) in 12. The results indicate that streptokinase applicated during a 6 hour-time window is a potent thrombolytic agent in acute myocardial infarction with limited effect on global left ventricular function. Pre-discharge evaluation is necessary to screen patients for residual ischemia.

Adult↗
PubMed1987

Relation between coronary artery stenosis and myocardial purine metabolism, histology and regional function in humans.

In 54 patients undergoing elective or emergency aortocoronary bypass grafting, angiographic and electrocardiographic changes were studied. Five patients with unstable angina and five patients with evolving myocardial infarction were included. High energy phosphate metabolism and the histologic appearance of the myocardium were analyzed in transmural biopsy specimens acquired at the time of surgery. In patients without anterior infarction on the electrocardiogram, severe stenosis of the left anterior descending coronary artery resulted in a reduction of anterior wall motion that was associated with a partial depletion of the adenylate pool. Mitochondrial function, however, remained intact: the adenosine diphosphate/adenosine triphosphate ratio, the energy charge and the creatine phosphate/adenosine triphosphate ratio were in the normal range. Histologic assessment demonstrated viable myocardium with a high incidence of atrophic cells. In evolving myocardial infarction, 170 minutes of acute coronary artery obstruction resulted in anterior wall akinesia associated with a decrease of the sum of the adenylates to 52% and of creatine phosphate to 16% of their normal value (p less than 0.05). The nucleosides accumulated; their major fraction (91%) was inosine. The adenosine diphosphate/adenosine triphosphate ratio increased from 0.14 +/- 0.04 to 0.49 +/- 0.20 (p less than 0.01) and the energy charge decreased from 0.924 +/- 0.021 to 0.660 +/- 0.169 (p less than 0.01). Ultrastructure examination revealed irreversible cell damage in at least the subendocardial layer. These results suggest that the energetic base of reduced contractility due to severe coronary artery stenosis is different from that in acute coronary obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Reduction in infarct size and enhanced recovery of systolic function after coronary thrombolysis with tissue-type plasminogen activator combined with beta-adrenergic blockade with metoprolol.

The effect of beta-adrenergic blockade on the salvage and functional recovery of reperfused myocardium was investigated in anesthetized dogs. Immediately after thrombotic occlusion of the left anterior descending coronary artery, the cardioselective beta-blocking agent metoprolol was given intravenously at a dose of 0.5 mg/kg infused over 10 min. One hour after the onset of occlusion, recanalization was initiated by intravenous infusion of recombinant human tissue-type plasminogen activator (rt-PA, 10 micrograms/kg/min for 30 min). Anatomic infarct size expressed as percent of the left ventricular mass (I/LV), global ejection fraction, and mean systolic shortening of the segmental radii (SS) of the infarcted area were measured either after 24 hr or 1 week in six groups of six dogs each: group I (rt-PA + metoprolol, evaluated at 24 hr), group II (rt-PA + metoprolol, evaluated at 1 week, group III (rt-PA alone, evaluated at 24 hr), group IV (rt-PA alone, evaluated at 1 week), group V (persistent occlusion, evaluated at 24 hr), and group VI (persistent occlusion, evaluated at 1 week). The smallest infarcts were found in reperfused dogs given metoprolol, but the differences from dogs receiving rt-PA alone were not statistically significant (I/LV, expressed as mean +/- SEM: 5.5 +/- 0.9% in group I, 6.7 +/- 1.9% in group II, 15.4 +/- 5.0% in group III, 11.4 +/- 3.5% in group IV, 23.6 +/- 2.5% in group V, and 26.9 +/- 2.3% in group VI).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Complete occlusion of the main left coronary artery. A clinical study.

Between 1975 and 1985, 12 patients with complete occlusion of the main left coronary artery (MLCA) were seen. The historical, clinical, biochemical, radiological, electrocardiographic, angiographical, surgical and follow-up findings were analyzed. Eight of the 12 patients presented on admission an unstable clinical situation. A normal ECG at rest was found in only 3 patients. Exercise testing elicited definite electrocardiographic changes in 5 of 6 cases. Coronary atherosclerosis was the cause of occlusion in 11 patients; in 1 patient the underlying disease process remained unclear. Significant lesions of the right coronary artery (RCA) were found in 9 and of the left anterior descending (LAD) or circonflex (CFLX) artery in 6 patients. Global and/or regional left ventricular dysfunction at rest was present in 10 patients. Angiographically visible collateral circulation was found in all patients but its extent was variable. All patients underwent bypass surgery. There were 1 operative and 2 late deaths.

Adult↗
PubMed1987

Emergency coronary bypass grafting for evolving myocardial infarction. Effects on infarct size and left ventricular function.

Emergency aorta-coronary bypass grafting was performed early in the course of evolving myocardial infarction in 48 patients. The time interval between the onset of symptoms and reperfusion was 169 +/- 80 minutes. Quantitative assessment of postoperative thallium 201 myocardial scans in 19 patients revealed a significant salvage of myocardium after surgical reperfusion: The size of the residual infarction was less than 50% of that in a matched, medically treated, prospective control group (n = 39) (p less than 0.05). Postoperative equilibrium-gated radionuclide blood pool studies (technetium 99m) showed an enhanced recovery of regional and global ejection fraction after operation as compared to after medical treatment (p less than 0.05). Ultrastructural evaluation of biopsy specimens obtained during the operation delineated subendocardial necrosis in the majority of cases (72%), but subepicardial necrosis was found in only 6% of instances. Q-wave abnormalities were observed on the postoperative electrocardiogram in 50% of cases. Operative mortality was 0% in low-risk patients (i.e., hemodynamically stable condition, n = 26) and 18% in high-risk patients (i.e., cardiogenic shock including total electromechanical dysfunction, n = 22). Survival rate at 18 months was 92% +/- 4%, and 95% +/- 4% of the survivors were event free. It is concluded that early surgical reperfusion of evolving myocardial infarction limits infarct size significantly, enhances functional recovery, and may be a lifesaving operation in patients having cardiogenic shock associated with unsuccessful resuscitation.

Actuarial Analysis↗
PubMed1986

Coronary thrombolysis by intravenous infusion of recombinant single chain urokinase-type plasminogen activator or recombinant urokinase in baboons: effect on regional blood flow, infarct size and hemostasis.

An occlusive thrombus was produced by thrombin-induced coagulation in the left anterior descending coronary artery of 18 open chest baboons. In six control animals, occlusive thrombosis persisting for 4 hours resulted in a large transmural infarct (66 +/- 4% of the perfusion area, mean +/- SEM). In six animals, single chain urokinase-type plasminogen activator, obtained by recombinant deoxyribonucleic acid (DNA) technology, was infused intravenously at a rate of 20 micrograms/kg per min for 60 minutes after approximately 45 minutes of coronary thrombosis. Persistent reperfusion occurred within 21 +/- 4 minutes (mean +/- SD). The mean duration of occlusion before reperfusion was 72 +/- 6 minutes. Recanalization resulted in a reduction of infarct size (42 +/- 4%, p less than 0.01 versus control animals). Myocardial blood flow in the perfusion area of the left anterior descending coronary artery was 107% of normal 2.5 hours after recanalization. The infusion of recombinant single chain urokinase-type plasminogen activator was not associated with systemic activation of the fibrinolytic system, fibrinogen breakdown or evident bleeding. In six baboons recombinant low molecular weight urokinase (molecular weight 33,000) was infused intravenously at a rate of 20 micrograms/kg per min for 60 minutes after approximately 45 minutes of coronary thrombosis. Persistent reperfusion occurred within 14 +/- 5 minutes (p less than 0.05 versus recombinant single chain urokinase-type plasminogen activator). The mean duration of occlusion was 69 +/- 14 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Coronary thrombolysis with recombinant tissue-type plasminogen activator: patency rate and regional wall motion after 3 months.

In a double-blind, placebo-controlled, randomized trial the long-term (+/- 3 months) effects of intravenous administration of recombinant tissue-type plasminogen activator (rt-PA) versus placebo were compared in relation to left ventricular function, coronary patency rate and antigenicity in 28 patients with a first myocardial infarction. Patency rate of the infarct-related coronary artery at the end of the rt-PA/placebo infusion and after 3 months of medical treatment (including oral anticoagulant agents) was 86 and 71%, respectively, in the rt-PA group, and 21 and 58%, respectively, in the placebo group. Regional wall motion of the infarct-related area was quantitated with digital subtraction angiography. Intrapatient comparisons revealed significant improvement in regional wall motion after 3 months in both the rt-PA and placebo groups. The improvement in the rt-PA group was not significantly greater than that in the placebo group. Thirteen patients (10 with rt-PA and 3 with placebo) with persistent patency (both early and late) of the infarct-related coronary artery showed a significant improvement of both global and regional left ventricular function, while 8 patients (2 with rt-PA and 6 with placebo) with persistent occlusion showed no changes. Antibodies against rt-PA were not detected in serum 2 weeks after the infusion, which is indicative of the lack of antigenicity of rt-PA and allows for its repeated administration.

Angiography↗
PubMed1986

Studies on experimental myocardial infarction: dogs or baboons?

The extrapolation to humans of results obtained in experimental studies is a major problem in cardiovascular research. It is generally believed that non-human primates provide a better model for the study of experimental myocardial infarction than the canine or porcine heart. In the present study the transmural distribution of myocardial infarction and collateral flow were compared between dogs and baboons. In the open chest model, the left anterior descending coronary artery was ligated for 4 h. In the subepicardial and subendocardial portions of the left ventricle myocardial blood flow was measured with tracer microspheres, and infarct size and site were determined using triphenyl tetrazolium chloride. In baboons, mean(SD) subendocardial collateral flow was higher than subepicardial collateral flow (41.8(24.6) ml . min-1 X 100 g-1 vs 28.6(21.3) ml . min-1 X 100 g-1 (p less than 0.05)). Subendocardial infarct size (expressed as a percentage of the perfusion area) was smaller than subepicardial infarct size (50.3(8.5)% vs 61.2(9.6)% (p less than 0.001)). In dogs, subendocardial collateral flow was less than subepicardial collateral flow (10.2(6.0) ml . min-1 vs 13.6(4.6) ml . min-1 X 100 g-1 (p less than 0.05)), and subendocardial infarct size was greater than subepicardial infarct size (67.3(12.9)% vs 38.3(18.0)% (p less than 0.01)). When, irrespective of the species or transmural localisation, infarct size is related to collateral flow, expressed as a percentage of normal flow, a weak but significant correlation is obtained (r = 0.61, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Coronary thrombolysis with recombinant single-chain urokinase-type plasminogen activator in patients with acute myocardial infarction.

Seventeen patients with acute transmural myocardial infarction and angiographically confirmed complete coronary occlusion were treated with heparin combined with intravenous single-chain urokinase-type plasminogen activator (scu-PA), obtained by expression of the cDNA encoding mature human scu-PA in Escherichia coli. In eight patients, recombinant scu-PA (rscu-PA) was given as a 10 mg bolus followed by 30 mg over 1 hr. Recanalization was obtained in six patients, but with persistent delayed opacification of the vessel in four of these patients. During infusion, a plateau level of rscu-PA antigen in plasma of 3.4 micrograms/ml (median value, range 1.4 to 5.5) was reached. At the end of the infusion the alpha 2-antiplasmin level had decreased to 54% (median, range 22% to 82%) of the preinfusion level, the fibrinogen level to 89% (median, range 26% to 101%), and fibrinogen degradation products (FDPs) to 20 micrograms/ml (median, range 8 to 387). In nine patients, rscu-PA was administered as a 10 mg bolus followed by 60 mg over 1 hr. This resulted in recanalization with normal distal filling of the vessel in seven patients, within 46 +/- 17 min (mean +/- SD). During infusion the concentration of rscu-PA in plasma increased to a median value of 7.4 micrograms/ml (range 4.0 to 13.3). At the end of the infusion the alpha 2-antiplasmin level was 22% of baseline (range 5% to 47%), the fibrinogen level 45% (range 4% to 94%), and the concentration of FDPs 87 micrograms/ml (range 6 to 1034). No significant bleeding or short-term side effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Coronary thrombolysis and infarct size reduction after intravenous infusion of recombinant tissue-type plasminogen activator in nonhuman primates.

Occlusive thrombus was produced by thrombin-induced coagulation in the left anterior descending coronary artery (LAD) of 16 open-chest baboons. In six control animals, occlusive thrombosis persisting over a period of 4 h as evidenced by coronary arteriography resulted in large transmural infarction (63.1 +/- 3.5% of the perfusion area). In 10 animals, tissue-type plasminogen activator obtained by recombinant DNA technology (rt-PA) was infused systemically at a rate of 1,000 IU (10 micrograms)/kg per min for 30 min after 30-80 min of coronary thrombosis. Reperfusion occurred within 30 min in nine animals. In one animal, intravenous infusion was followed by an intracoronary infusion at the same rate, which resulted in thrombolysis within 8 min. In the rt-PA group, mean duration of occlusion before reperfusion was 77 +/- 24 min. Reocclusion occurred in one animal. Recanalization resulted in an overall reduction of infarct size (37.8 +/- 5.9%, P less than 0.05 versus controls). Residual infarction was related to the duration of occlusion (r = 0.80, P less than 0.01). Reperfusion was associated with reduced reflow. Myocardial blood flow in the perfusion area of the LAD was only 70% of normal after 4 h despite perfect angiographic refilling. The infusion of rt-PA was not associated with systemic activation of the fibrinolytic system, fibrinogen breakdown, or clinically evident bleeding. It is concluded that intravenous infusion of rt-PA may recanalize thrombosed coronary vessels without inducing systemic lysis. The extent of residual infarction is closely related to the duration of coronary artery occlusion before thrombolysis.

Angiography↗