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C J Vrints

Publications and source records attributed to C J Vrints.

At least 37 records · Page 2Linked to original sources
PubMed1998

User-friendly and low-cost computer system for immediate review, analysis, and reconstruction of intracoronary ultrasound images.

Rapid review, digital recording, on-line quantification, and three-dimensional reconstruction are all essential in the evaluation of intracoronary ultrasound images during coronary interventions. We describe a low-cost method that offers all these necessary features. The proposed method uses the QuickTime compatible video digitizers of standard multimedia Apple Macintosh or PowerPC desktop computers and the freeware software Object Image 1.60.

Computer Systems↗
PubMed1998

Primary pulmonary hypertension in a patient with HIV infection.

Several case-reports and small series suggest a causal relationship between human immunodeficiency virus (HIV) infection and pulmonary hypertension. We report on a HIV seropositive man with a high and stable CD4 lymphocyte count (+/- 600/mm3) who developed severe pulmonary hypertension, not attributable to other known causes. This case report underscores the fact that the degree of immunosuppression secondary to the HIV-infection seems to be of little relevance in the pathophysiology of the syndrome. HIV-infected patients with dyspnoea, not related to pulmonary infection, with exercise intolerance, syncope or precordial pain should receive an electrocardiogram and echocardiographic assessment. The exact pathogenetic mechanism of this rapidly progressive disease and whether anti-viral therapy should be promoted is still under investigation.

Adult↗
PubMed1997

Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction. Paradoxical scintigraphic underestimation of jeopardized myocardium in patients with a severe infarct-related stenosis.

This study investigated the value of technetium-99m sestamibi scintigraphy in identifying patients at risk for post-infarct ischaemia (=jeopardized myocardium), especially within the reperfused infarct region. In 51 patients with a recent (<1 month) myocardial infarction, adenosine 99mTc-sestamibi single-photon emission tomography (SPET) and dobutamine stress echocardiography (DSE) were performed and correlated with the presence of significant coronary artery stenosis [% diameter stenosis (DS) >50%] on quantitative coronary angiography. Regional perfusion activity was analysed semi-quantitatively (score 0-4) on a 13-segment left ventricular model. DSE was used for the estimation of the infarct size (low-dose DSE) and for concomitant evaluation of ischaemia (high-dose DSE). A reversible perfusion defect within the infarct region was observed in 20 of the 37 patients with a significant infarct-related lesion (sensitivity of 54%) and only in one patient without a significant infarct-related lesion (specificity of 93%). Further analysis revealed that the scintigraphic assessment of jeopardized myocardium was fairly good in patients with a moderate (DS 51%-64%) infarct-related stenosis but was inadequate in patients with a severe (DS>/=65%) infarct-related stenosis (sensitivity of 80% vs 36%, P<0.01), while the echocardiographic detection of ischaemia was not influenced by stenosis severity (sensitivity of 73% in both subgroups). This scintigraphic underestimation of jeopardized myocardium was mainly related to a severely impaired myocardial perfusion under baseline conditions, as was evidenced by a significantly more severe rest perfusion score in the infarct region in patients with a severe stenosis as compared to those with a moderate stenosis (average score: 1.5+/-0.7 vs 2.1+/-0.6, P<0.01), while infarct size on echocardiography was similar for both subgroups. It may be concluded that early after an acute myocardial infarction, adenosine 99mTc-sestamibi SPET may underestimate reperfused but still jeopardized myocardium, particularly in patients with a severe infarct-related stenosis. In these patients the evaluation of the ischaemic burden on rest-stress scintigraphy is hampered by the presence of a severely impaired myocardial perfusion in resting conditions.

Adenosine↗
PubMed1997

Fibrin(ogen) and von Willebrand factor deposition are associated with intimal thickening after balloon angioplasty of the rabbit carotid artery.

The aim of the study was to assess the contribution of thrombus incorporation into neointimal thickening in the rabbit carotid artery after deep vascular injury induced by balloon angioplasty compared with superficial vascular injury induced by a perivascular collar. Besides CD 31 (PECAM 1), vimentin, alpha-smooth muscle actin, rabbit anti-macrophage monoclonal antibody and proliferating cell nuclear antigen, fibrin(ogen) and von Willebrand factor (vWF) deposition was assessed immunohistochemically. Angioplasty was performed in 47 rabbits and evaluated immediately (n = 7), after 6 hours (n = 4), and after 1 (n = 7), 2 (n = 9), or 3 (n = 20) weeks. A collar was placed in 29 rabbits and evaluated immediately (n = 5), after 6 hours (n = 5), and after 1 (n = 7), 2 (n = 10), or 3 (n = 2) weeks. After dilatation, the arteries were extensively denuded of endothelium, the internal elastic membrane was ruptured and blood-filled clefts were present in the media, pointing to deep vascular (type III) injury. Six hours later, mural fibrin(ogen) thrombi were formed, specially at sites with severe damage. This fibrin(ogen) matrix became infiltrated by phagocytes and smooth muscle cells. A luminal cap covered by regenerating endothelium was formed, demonstrating increased immunoreactivity to vWF. vWF was deposited in the extracellular neointimal spaces. Fibrin(ogen) thrombus deposition and incorporation appeared to be protracted phenomena for at least 2 weeks. After collar placement, minimal endothelial denudation was documented, pointing to focal superficial (type I) vascular injury. In subsequent weeks, neointimal thickening was associated with vWF deposition but not with fibrin(ogen) thrombus incorporation. In conclusion, mural fibrin(ogen) thrombus formation and incorporation contribute to neointima formation after deep vascular injury and seem to occur for several weeks after the initial insult.

Actins↗
PubMed1996

Balloon angioplasty and induction of non-endothelial nitric oxide synthase in rabbit carotid arteries.

The purpose of the study was to evaluate whether balloon angioplasty is associated with changes in nitric oxide synthase (NO synthase) activity. Normal rabbit carotid arteries were examined 10 min or 1, 2, 3 or 10 weeks after angioplasty with 2 or 2.5-mm balloons. Immunohistology was used to evaluate intimal thickening and endothelial cell regeneration. The NO synthase activity was studied functionally using isolated segments in organ chambers. Immunohistochemistry of the endothelial cell markers von Willebrand factor and platelet endothelial cell adhesion molecule-1 indicated that the regeneration of endothelial cells from patchy islands that remained after angioplasty was virtually complete within 2 weeks. However, the endothelium-dependent relaxations elicited by acetylcholine remained impaired up to 10 weeks after dilation. Contractions elicited by 5-hydroxytryptamine (5-HT) were attenuated, but were significantly augmented by the NO synthase blocker, nitro-L-arginine. Furthermore, in contrast to normal arteries, the balloon-treated arteries developed marked contractions in response to nitro-L-arginine methyl ester (L-NAME), contractions which could be reversed by L-arginine. The latter contractions and relaxations were not influenced by endothelial removal. These results suggest that although the endothelium quickly regenerates after severe balloon injury, the endothelium-dependent release of nitric oxide remains disturbed. However, the functional data also suggest that angioplasty led to a significant induction of NO synthase in 'non-endothelial' cells of the artery.

Angioplasty, Balloon↗
PubMed1996

Comparative study of rest technetium-99m sestamibi SPET and low-dose dobutamine stress echocardiography for the early assessment of myocardial viability after acute myocardial infarction: importance of the severity of the infarct-related stenosis.

Rest technetium-99m sestamibi single-photon emission tomography (SPET) has been shown to underestimate viability in some patients with chronic ischaemic myocardial dysfunction. The present study was designed to appraise the value of 99mTc-sestamibi as a viability tracer in patients with a recent myocardial infarction and to determine factors that might influence its accuracy in assessing infarct size. Therefore, rest 99mTc-sestamibi SPET, low-dose dobutamines stress echocardiography and quantitative coronary angiography were performed in 51 patients with a recent myocardial infarction. Perfusion activity and regional wall motion were scored semi-quantitatively using the same segmental division of the left ventricle. Assessment of 99mTc-sestamibi uptake as a marker of viability was performed by comparing a binary uptake score (viable=>50% vs necrotic =</=50% of the maximal tracer activity) with a binary wall motion classification during low-dose dobutamine infusion (viable=normal/hypokinetic vs necrotic=akinetic/dyskinetic). Infarct size, expressed as the number of segments with evidence of necrotic tissue, was significantly greater in the scintigraphic study than in the echocardiographic study (2.8+/-1.5 vs 2.2+/-1.3, P=0.006). This overestimation of infarct size by 99mTc-sestamibi was present only in patients with a severe infarct-related stenosis (% diameter stenosis >/=65%-100%) and particularly those with "late" reperfusion therapy (time delay >/=180 min). In patients without a severe infarct-related stenosis, 99mTc-sestamibi was able to accurately distinguish viable from necrotic segments. Thus, rest 99mTc-sestamibi scintigraphy early after acute myocardial infarction may underestimate residual viability within the infarct region, particularly in patients with low flow state coronary anatomy, as a result of a severe infarct-related stenosis and/or late reperfusion therapy.

Cardiotonic Agents↗
PubMed1996

Coronary flow reserve during coronary angioplasty in patients with a recent myocardial infarction: relation to stenosis and myocardial viability.

OBJECTIVES: In the present study, we examined post-stenotic coronary flow before and after percutaneous transluminal coronary angioplasty (PTCA) in patients with and without a recent myocardial infarction (MI) and related it to stenosis severity and residual viability. BACKGROUND: Post-stenotic coronary blood flow velocity reserve (CFVR) has been used with success to estimate functional stenosis severity in patients with stable angina. However, in patients with a recent MI, the impaired coronary vasodilator response of the reperfused myocardium may substantially alter the flow dynamics of the infarct-related artery. METHODS: Distal coronary flow velocities were recorded before and after PTCA in 36 patients at day 13 +/- 7 (mean +/- SD) after acute MI and in 38 patients without MI. The CFVR was assessed by the ratio of distal hyperemic to baseline average peak velocity, using a 0.014-in. Doppler guide wire. Stenosis severity was analyzed by quantitative coronary angiography, and infarct size was assessed scintigraphically. RESULTS: For similar angiographic stenosis severity, pre- and post-PTCA values of CFVR were significantly lower in patients with than without MI: 1.22 +/- 0.26 versus 1.50 +/- 0.45 before PTCA (p < 0.05) and 1.72 +/- 0.43 versus 2.21 +/- 0.74 after PTCA, respectively (p < 0.01). Although CFVR increased significantly (p < 0.0001) after angiographically successful PTCA in both study groups, abnormal CFVR (< or = 2.0) was still observed in 80% of patients with MI and in 44% of those without MI (MI vs. no MI, p = 0.001). Patients with an extensive infarction (relative infarct size > or = 50%) and those with a small infarction (relative infarct size < 50%) had comparable levels of post-PTCA CFVR (1.6 +/- 0.3 vs. 1.8 +/- 0.5, p = NS). Among a variety of factors, angiographic stenosis severity was the most important determinant of CFVR in both study groups. CONCLUSIONS: In patients with a recent MI, CFVR was significantly lower than in those without MI, both before and after PTCA. Besides the presence of this postreperfusion-related impairment of the coronary vasodilating response, CFVR was mainly influenced by stenosis severity and not by residual viability.

Adult↗
PubMed1996

Aminophylline inhibits adaptation to ischaemia during angioplasty. Role of adenosine in ischaemic preconditioning.

UNLABELLED: The ability of brief periods of ischaemia to protect the heart from subsequent ischaemia has been termed "ischaemic preconditioning'. In order to assess the role of adenosine receptor stimulation in this phenomenon we studied the ischaemic preconditioning effect during angioplasty in 10 control patients and in 10 patients pre-treated with 5 mg.kg-1 aminophylline, an adenosine receptor antagonist. The ischaemic response was assessed by analysis of the intracoronary electrocardiogram every 10 s during three consecutive inflations of 90 s with a reperfusion time of 180 s. The severity of transmural local ischaemia was expressed as the magnitude of the ST segment shift in relation to the time during each inflation. The control patients showed an improved tolerance to myocardial ischaemia: ST segment shift decreased from 1.42 +/- 0.49 mV at the end of the first inflation to 1.03 +/- 0.44 mV at the end of the third inflation (P < 0.001). However, in patients pre-treated with aminophylline, the ischaemic response was not significantly different during three inflations. CONCLUSION: Aminophylline inhibits ischaemic preconditioning, as assessed by analysis of the intracoronary. ST segment changes during angioplasty. This suggests that ischaemic preconditioning is mediated by adenosine receptor stimulation in humans.

Adaptation, Physiological↗
PubMed1996

Clinical outcome of patients with an uncomplicated myocardial infarction: effect of revascularization.

In 80 patients (pts) with an uncomplicated myocardial infarction (MI) the rate of major cardiac events (MACE) including cardiac death, non-fatal myocardial infarction and recurrent ischemia requiring hospitalization was prospectively assessed over a mean follow-up period of 17 +/- 9 months and related to clinical, angiographic and scintigraphic findings, the latter obtained from adenosine Tc-99m sestamibi SPECT imaging. Decision for revascularization was mainly based on angiographic data and was carried out in a total of 50 patients (angioplasty in 34 pts and cardiac surgery in 16 pts). The overall MACE rate was 24% with a mortality and myocardial infarction rate of 4% and 5%, respectively. Early (< 2 months) revascularization seemed to have a beneficial effect on clinical outcome as was suggested by the following findings: 1) Cardiac events (MACE) were not significantly different in patients with versus without revascularization (MACE 24% versus 23%) although the former constituted a subgroup at higher risk for ischemic events because of a more extensive coronary artery disease state. 2) In the subset of patients with at least one significant coronary artery stenosis the clinical outcome was significantly better in those who were revascularized than in those who underwent no revascularization (MACE 24% vs 47%, p < 0.05. Among a variety of factors, including the scintigraphic and angiographic extent of coronary artery disease and post-MI treatment strategy, multivariate analysis selected hypercholesterolemia (> 240 mg%) as the only independent predictor of MACE with a more than fourfold increase in risk for development of MACE. These data suggest that the natural history, especially the rate of recurrent ischemic events, can be favourably changed by an elective and early revascularization, strategically oriented by the results of the angio-graphic study. Furthermore, our data emphasized the deleterious role of hypercholesterolemia on clinical outcome in patients with a recent MI.

Angioplasty, Balloon, Coronary↗
PubMed1995

Adenosine technetium-99m sestamibi (SPECT) for the early assessment of jeopardized myocardium after acute myocardial infarction.

The purpose of this study was to evaluate the accuracy of adenosine Tc-99m sestamibi single photon emission computed tomography (SPECT) in the detection of jeopardized myocardium early after acute myocardial infarction. Coronary arteriography and myocardial scintigraphy were performed in 50 consecutive patients with an uncomplicated myocardial infarction. Myocardium was considered jeopardized if a significant infarct-related vessel stenosis (> 50% diameter stenosis) supplied an infarct area with residual viable tissue. Perfusion reversibility in the infarct region occurred in 25 patients (50%) and was almost solely observed in the presence of jeopardized myocardium. Non-reversible perfusion defects in the infarct region were found in patients without jeopardized myocardium. This subgroup consisted of either patients without significant vessel stenosis or patients without significant residual viability in the infarct region. Adenosine Tc-99m sestamibi SPECT had an accuracy of 88% for the detection of jeopardized myocardium. Side effects during adenosine infusion were frequently observed but well tolerated. These results suggest that adenosine Tc-99m sestamibi SPECT is an accurate non-invasive method for detecting jeopardized myocardium after acute myocardial infarction and may be a valuable non-invasive test for the early selection of patients at risk for future ischaemic events.

Adenosine↗
PubMed1995

Isosorbidedinitrate and SIN-1 as dilators of human coronary arteries and platelet inhibitors.

We compared isosorbidedinitrate (ISDN) and 3-morpholinosydnonimine (SIN-1) as dilators of epicardial coronary arteries and inhibitors of ex vivo platelet aggregation in 23 patients referred for diagnostic coronary arteriography. After completion of the diagnostic study, the patient received graded intravenous (i.v.) infusions (0.5, 1.0, and 1.5 micrograms/kg/min) of either SIN-1 (n = 11) or ISDN (n = 12). Diameters of left anterior descending (LAD) and left ramus circumflex (RCX) coronary arteries were assessed by quantitative digital coronary arteriography before and 5 min after each infusion was started. SIN-1 required an infusion rate of 1.0 micrograms/kg/min to cause dilatation of proximal and middle segments of LAD and RCX. The highest infusion rate caused a modest decrease in mean arterial blood pressure (MAP). In these aspects, SIN-1 was equivalent to ISDN. In addition, blood was collected immediately before treatment and after infusion of the highest dose of ISDN or SIN-1. The sensitivity of platelet-rich plasma (PRP) to ADP and the thromboxane A2 (TXA2) mimetic U-46619 was determined in an aggregometer. The lesser responses to threshold concentrations of ADP and U-46619 and the slight shift in both concentration-response curves indicated that platelets of SIN-1-treated patients were slightly less sensitive to both stimuli as compared with platelets of ISDN-treated subjects. These ex vivo results suggest that SIN-1 may be superior to ISDN as an inhibitor of platelet activation.

Angina Pectoris↗
PubMed1994

Paradoxic pulmonary vasoconstriction in response to acetylcholine in patients with primary pulmonary hypertension.

Pulmonary vascular reactivity was assessed during diagnostic heart catheterization in two patients with pulmonary hypertension unexplained by pulmonary or cardiac disease and in five patients with atypical chest pain and normal coronary arteriograms. Acetylcholine, an endothelium-dependent vasodilator that also has a direct contracting effect on vascular smooth muscle cells, was infused in the right atrium in a step-wise increasing dose in order to obtain final blood concentrations in the pulmonary circulation ranging from 10(-6) mol/L to 10(-4) mol/L. In the five control patients, acetylcholine induced a dose-related decrease of pulmonary vascular resistance (-52 percent +/- 9 percent). In the patients with primary pulmonary arterial hypertension, however, acetylcholine caused a paradoxic increase of pulmonary arterial pressure and of pulmonary vascular resistance. Thus, it appears that endothelium-dependent vasodilation is impaired in the pulmonary circulation of patients with primary pulmonary arterial hypertension. Endothelial dysfunction in the pulmonary circulation may play a role in the pathophysiology of this disease.

Acetylcholine↗
PubMed1992

Impaired endothelium-dependent cholinergic coronary vasodilation in patients with angina and normal coronary arteriograms.

The coronary vasomotor responses to selective infusion of graded concentrations (10(-6) to 10(-4) M) of acetylcholine into the left anterior descending artery were assessed by quantitative coronary arteriography in 24 patients with normal coronary arteriograms (12 patients with atypical symptoms and 12 patients with typical anginal pain) and 36 patients with coronary artery disease with different degrees of atherosclerosis of the left anterior descending artery. In the patients with normal coronary arteries and atypical chest pain, acetylcholine induced predominantly a vasodilator response, which was maximal during a 10(-5) M acetylcholine infusion. In contrast, in patients with coronary artery disease, acetylcholine caused dose-dependent vasoconstriction, which was observed even if the left anterior descending artery itself was smooth. Marked vasoconstriction was also induced in the patients with typical anginal pain and angiographically normal coronary arteries. In nine of these patients, this constrictor response was associated with anginal pain and electrocardiographic evidence of myocardial ischemia. Intracoronary administration of isosorbide dinitrate (1 mg) relieved the anginal pain and dilated all vessels. These data suggest that 1) patients with normal coronary arteriograms and angina pectoris manifest impairment of endothelium-dependent vasodilation similar to that observed in patients with overt coronary atherosclerosis; and 2) abnormal coronary vasoconstrictor responses resulting from this impairment may contribute to the pathogenesis of myocardial ischemia and angina in these patients.

Acetylcholine↗
PubMed1992

Paradoxical vasoconstriction as result of acetylcholine and serotonin in diseased human coronary arteries.

UNLABELLED: In experimental atherosclerosis, impairment of endothelium-dependent vasodilation results in an unmasking of potent vasoconstrictor responses to serotonin, a substance released by aggregating platelets. To determine whether similar changes occur in diseased human coronary arteries, the responses to selective intracoronary infusions of acetylcholine and serotonin (both endothelium-dependent vasodilators) and to isosorbide dinitrate (a dilator directly acting on the smooth muscle) were assessed by quantitative coronary arteriography in 16 patients with angiographically normal coronary arteries, in 10 patients with minimal (less than 30% narrowing) and in five patients with more advanced (greater than 50% narrowing) coronary atherosclerosis. Acetylcholine induced constriction in diseased coronary arteries, but in patients with normal coronary arteriograms, it caused dilatation in seven patients (smooth dilators) and constriction in nine patients (smooth constrictors). In the smooth dilators, however, serotonin evoked no significant changes (+1.4 +/- 4.1%), whereas in the smooth constrictors and in patients with diseased coronary arteries, serotonin caused dose-dependent constriction. The vasoconstrictor responses to serotonin were similar in patients with minimal (-26.5 +/- 4.7%) and more advanced atherosclerosis (-30.9 +/- 5.3%). In one patient with coronary artery disease, serotonin caused a temporary coronary occlusion. All other patients dilated in response to isosorbide dinitrate. The vasomotor responses to acetylcholine and to serotonin were thus shown to be completely in parallel. CONCLUSION: impairment of endothelium-dependent vasodilation unmasks potent vasoconstrictor responses to serotonin both in early and advanced coronary atherosclerosis. These changes may play an important role in the pathogenesis of a dynamic coronary artery stenosis.

Acetylcholine↗
PubMed1992

Angiographic coronary artery lesion morphology and pathogenetic mechanisms of myocardial ischemia in stable and unstable coronary artery disease syndromes.

The angiographic morphology of coronary artery stenoses was studied in 160 patients referred for diagnostic coronary arteriography. Three groups of patients were studied: 60 patients with stable angina, 78 patients with unstable angina and 22 patients with a recent myocardial infarction. Complex lesions were more frequently observed in patients with unstable angina (59%, p less than 0.001) and in patients with a recent myocardial infarction (54%, p less than 0.05) then in patients with stable angina (25%). Angiographic signs suggestive for the presence of intravascular thrombi were almost exclusively observed in the patients with unstable angina (34%, p less than 0.001) and in the patients with a recent myocardial infarction (27%, P less than 0.001) and were almost completely absent in the patients with stable angina (1.5%). The high prevalence of complex coronary artery lesion morphology and of intravascular thrombi observed in patients with unstable angina or with a recent myocardial infarction emphasizes the important role of intima disruption and of subsequent thrombosis in the pathogenesis of myocardial ischemia in those unstable syndromes of ischemic heart disease.

Angina Pectoris↗