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C J Vrints

Publications and source records attributed to C J Vrints.

At least 19 recordsLinked to original sources
PubMed2001

Screening for solid organ malignancies prior to heart transplantation.

BACKGROUND: Prognosis of solid organ cancer in immunosuppressed hosts is generally dismal. Therefore, every effort to identify patients with asymptomatic carcinomas before transplantation should be encouraged. METHODS: Sixty-seven patients referred for heart transplantation were examined adhering to the scheme proposed at the 24th Bethesda Conference. To increase the sensitivity of this work-up, the following items were added: tumor marker assays (prostate-specific antigen in males, carcino embryogenic antigen), abdominal ultrasound, CT scan of the abdomen and the thorax, mammography/echography of the breasts, PAP smear, colonoscopy if carcino embryogenic antigen abnormal or occult blood in stool, prostate echography if prostate-specific antigen abnormal or prostate hypertrophy. RESULTS: Carcinoma was detected in 10 of the 67 patients; for 8 patients of this cancer group, transplantation was denied. Importantly, 9 of the 10 malignancies were detected by means of the diagnostic items that were added to the standard screening protocol. There were no significant differences between the cancer and the non-cancer group regarding mean age, sex, etiology of heart failure, and smoking history. Stratifying patients in younger (i.e., < or =54 years) and older (i.e., > or =55 years) age groups showed a significantly greater proportion of older patients in the cancer group (8/10=80%) compared to the non-cancer group (25/57=44%), P=0.04. After a mean follow-up of 34 months, 5 of the 36 transplanted patients developed a malignancy (4 skin carcinomas, 1 non-Hodgkin lymphoma). There have been no malignancy-related deaths until now. CONCLUSION: The importance of a thorough screening program in the triage of candidates with preexisting malignancies, especially in an older patient population, is illustrated in this report.

Adult↗
PubMed2001

Reliability of fractional flow reserve measurements in patients with associated microvascular dysfunction: importance of flow on translesional pressure gradient.

Fractional flow reserve (FFR) has been applied with success as a lesion-specific functional indicator of stenosis severity, at least in patients with normal microcirculation. This study sought to assess the reliability of FFR calculations in patients with associated microvascular dysfunction (e.g., post myocardial infarction, or post-MI). First, the effect of coronary flow changes on translesional pressure gradient was assessed. Therefore, intracoronary pressure and flow was recorded simultaneously across 19 non-infarct-related lesions (both pre- and postinterventional lesions with a mean diameter stenosis of 47% +/- 12%). Measurements were performed by means of a pressure and Doppler wire during maximal hyperemia and also during submaximal hyperemia induced by low-dose adenosine. The drop of coronary flow from 48 +/- 23 ml/min during maximal hyperemia to 36 +/- 18 ml/min during submaximal hyperemia was associated with a small decrease in translesional pressure gradient (from 22 +/- 12 mm Hg to 19 +/- 12 mm Hg; P = 0.02) and a small increase in the mean distal/arterial pressure ratio (Pd/Pa) going from 77% +/- 11% to 81% +/- 11% (P = 0.003). Then, intracoronary pressure and flow measurements were compared across 21 non-infarct-related lesions vs. 22 matched infarct-related lesions. For a similar angiographic stenosis severity (% DS = +/- 44%), maximal flow was 48 +/- 22 ml/min in the non-infarct arteries and 37 +/- 26 ml/min in the infarct arteries (P = 0.03), confirming the presence of severe microvascular dysfunction in infarct regions. Similar to the earlier findings, this hyperemic flow reduction in MI patients was associated with a small increase of FFR (= Pd/Pa): 79% +/- 12% in no MI vs. 83% +/- 12% in MI patients (P = 0.3). A reduction of hyperemic flow by +25%, [correction] such as can be found in patients with severely impaired microvascular function, has a limited effect on FFR calculations (+ 5%). This finding allows the application of standard FFR calculations in a more general population of ischemic heart disease, including patients with recent MI.

Aged↗
PubMed2000

Successful recovery after ventricular fibrillation in a patient with Kawasaki disease.

Kawasaki disease (KD) is an uncommon cause of sudden death in young adults in Europe. Angiographically, the disease is characterized by coronary artery aneurysms which can be fully obstructed by acute thrombosis or by progression of the disease. If diagnosis of KD is made, immediate investigation should be made to determine whether ischemia is occurring and if so, to establish optimal time for revascularisation or cardiac transplantation. We describe an 18-year-old Caucasian male who was not previously known to have KD and who suffered from an acute myocardial infarction complicated by ventricular fibrillation, caused by acute thrombosis of a coronary artery aneurysm.

Adolescent↗
PubMed1999

Inducible nitric oxide synthase colocalizes with signs of lipid oxidation/peroxidation in human atherosclerotic plaques.

OBJECTIVE: Advanced human atherosclerotic plaques are characterized by the abundant presence of the autofluorescent non-soluble lipid pigment ceroid, consisting of oxidized lipoproteins. The aim of the present study was to examine the topographical and cellular distribution of inducible nitric oxide synthase (iNOS or NOS II) within different stages of atherosclerosis and its colocalization with ceroid deposits and nitrotyrosine. METHODS AND RESULTS: Different stages of atherosclerosis were studied by immunohistochemistry on whole-mount longitudinal sections of carotid endarterectomy specimens. In the adaptive intimal thickening the predominant cell type were smooth muscle cells. The fatty streaks contained both smooth muscle cells and macrophages with an extremely low NOS II immunoreactivity. The advanced atherosclerotic plaques however, showed a very dense infiltration by macrophages, of which a subpopulation expressed NOS II as a vesicular immunoreactivity in their cytoplasm. These were mainly present around the necrotic core, in association with ceroid accumulation and nitrotyrosine. Fluorescence quenching microscopy showed the presence of NOS II on autofluorescent ceroid vesicles in the macrophages. Large extracellular ceroid granules were not NOS II immunoreactive. NOS II mRNA was detected by RT-PCR and the protein by Western blot in the plaque tissue but not in mammary arteries used as controls. CONCLUSION: Ceroid, nitrotyrosine and NOS II colocalized in late stages of atherosclerosis and were found around the necrotic core in the plaque. This could suggest that NOS II expression in macrophages is involved in oxidation and peroxidation of lipids, leading to ceroid formation.

Aged↗
PubMed1999

Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome.

BACKGROUND: Despite early recanalization of an occluded infarct artery, reperfusion at the level of the microcirculation may remain impaired owing to a process of microvascular reperfusion injury. METHODS AND RESULTS: Microvascular reperfusion injury was studied in 91 patients with acute myocardial infarction (AMI) by evaluation of the resolution of ST-segment elevation after successful PTCA. Impaired microvascular reperfusion, defined as the presence of persistent (>/=50% of initial value) ST-segment elevation (ST >/=50%) at the end of coronary intervention, was observed in 33 patients (36%) and was independently correlated with low systolic pressure on admission and high age. Patients >/=55 years of age with systolic pressures </=120 mm Hg were at high risk for development of impaired reperfusion compared with patients not meeting these criteria (72% versus 14%, P<0.001). Impaired microvascular reperfusion was associated with a more extensive infarction and worse clinical outcome at the 1-year follow-up: cardiac death rate, 15% versus 2% (ST >/=50% versus ST <50%, P=0.01); nonfatal MI rate, 9% versus 2% (P=0.1); and total major adverse cardiac event (MACE) rate, 45% versus 15% (P<0.005). ST >/=50% was the most important independent determinant of MACE with an adjusted risk ratio of 3.4. CONCLUSIONS: Impaired microvascular reperfusion, as evidenced by ST >/=50% after successful recanalization, occurs in more than one third of our AMI patients, especially in older patients with low systolic pressure. Its detrimental implications on clinical outcome reinforce the need to develop adjunctive agents that attenuate the process of reperfusion injury.

Aged↗
PubMed1999

Effect of stenting on coronary flow velocity reserve: comparison of coil and tubular stents.

OBJECTIVE: To determine whether coil stents are as effective as tubular stents in improving coronary flow velocity reserve (CFVR) after stent deployment. METHODS: Distal CFVR was measured with a 0. 014 inch Doppler guide wire before and after stenting in 33 patients. A coil stent was implanted in 16 patients and a tubular stent was used in 17 patients. Coronary flow velocity within the stent was also recorded during a slow pullback. RESULTS: Following placement of the stents, the percentage diameter stenosis was similar for both the tubular and coil stents (mean (SE) 11 (2)% v 13 (2)%, NS). However, distal CFVR was higher after stenting with a tubular stent compared with a coil stent (2.46 (0.13) v 1.96 (0.14), p < 0.05). Furthermore, pullback through the stent detected a major flow velocity increase within coil stents but not in tubular stents (83 (24)% v 5 (5)%, p < 0.05). CONCLUSIONS: In spite of similar angiographic improvement, placement of coil stents was associated with inferior functional results compared with tubular stents. The flow velocity acceleration within the coil stents suggests the presence of a residual narrowing within the stent, which is not appreciated on angiography.

Analysis of Variance↗
PubMed1999

Continuous perivascular L-arginine delivery increases total vessel area and reduces neointimal thickening after experimental balloon dilatation.

The aim of this study was to evaluate whether vascular remodeling and neointimal thickening occur after balloon dilatation of the nonatherosclerotic rabbit carotid artery, and whether both processes are influenced by continuous perivascular delivery of L-arginine or the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). In the first experiment, histological and morphometric evaluation of arteries was performed at different time points after balloon dilatation: 10 minutes (n=7), and 1 (n=7), 2 (n=9), 3 (n=20), or 10 (n=5) weeks. Neointimal thickening progressively contributed to luminal narrowing for at least 10 weeks after angioplasty. During the first 2 weeks after dilatation, a significant decrease of the total vessel area was measured. Ten weeks after dilatation, both the neointimal and total vessel area were increased without further changing of the luminal area. In the second experiment, endothelial injured rabbits were randomly assigned to receive 2 weeks of continuous local perivascular physiological salt solution (n=6), L-arginine (n=8), or L-NAME (n=7), starting immediately after balloon dilatation (ie, local drug delivery during the first phase of the biphasic vascular remodeling process). Perivascular L-arginine delivery significantly reduced the neointimal area, despite an increased number of neointimal Ki-67-positive smooth muscle cells. Both the luminal area and total vessel area were significantly increased. Serum L-arginine levels remained unchanged. L-NAME administration had no effect on the neointimal area, nor on the luminal and total vessel area. Neointimal formation and biphasic vascular remodeling occur after experimental balloon dilatation of the nonatherosclerotic rabbit carotid artery, and can be influenced by continuous local perivascular delivery of L-arginine.

Animals↗
PubMed1999

Spontaneous dissection of three major coronary arteries subsequent to cystic medial necrosis.

This case report describes the devastating consequences of spontaneous coronary dissection in a 36-year-old female patient. Surgical revascularization was attempted, but diffuse myocardial infarction developed. The patient was bridged to heart transplantation but died secondary to multiple organ failure. To our knowledge, this is the only reported case of spontaneous dissection of the three main coronary arteries due to severe cystic medial necrosis.

Adult↗
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↗