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Biomedical subjects

M Vanderheyden

Publications and source records attributed to M Vanderheyden.

At least 19 recordsLinked to original sources
PubMed2006

Head to head comparison of N-terminal pro-B-type natriuretic peptide and B-type natriuretic peptide in patients with/without left ventricular systolic dysfunction.

BACKGROUND: Human pro-B-type natriuretic peptide is cleaved into the active B-type natriuretic peptide (BNP) and the inactive fragment NT-proBNP. It is unclear if, similar to BNP, NT-proBNP can be used as a marker of impaired left ventricular (LV) ejection fraction (EF). This study evaluated the analytical performance of both assays to detect LV systolic dysfunction. METHODS: In 72 patients with various degrees of left ventricular systolic dysfunction (LVSD), blood analysis for BNP and NT-proBNP was performed prior to cardiac catheterization, using a point-of-care analyzer (Biosite) and a fully automated laboratory analyzer (Roche-Elecsys), respectively. The within-run and between-run imprecision for BNP and NT-proBNP was calculated. RESULTS: Both markers were able to detect impaired LV EF with the largest area under the receiver-operating-characteristic curve for NT-proBNP (NT-proBNP: 0.851 (0.747-0.924); BNP: 0.803 (0.692-0.887) 95% confidence interval; P = 0.07). A significant correlation was observed between BNP and NT-proBNP (r = 0.9; P < 0.0001). Estimating the within-run imprecision, the coefficient of variance for BNP was 3.14% (n = 20, mean 316 ng/L) to 3.32% (n = 20, mean 820 ng/L) and for NT-proBNP 0.9% (n = 20, mean 4390.8 ng/L) to 1.4% (n = 20, mean 225 ng/L). The between-run imprecision for NT-proBNP ranged between 2.1% (n = 20, mean 224.6 ng/L) and 2% (n = 20, mean 4391 ng/L). Optimal discriminator values for BNP and NT-proBNP were 139 ng/L and 358 ng/L, respectively. However, adjusting the BNP cut-off value to 54 ng/L improved the negative predictive value and sensitivity of the assay. CONCLUSION: Similar to BNP, NT-proBNP is a promising marker in identifying LVSD. Although both assays are reliable and have good analytical performance, their diagnostic cut-off value is dynamic and population-dependent. The slightly wider detection range and the more stable structure of NT-proBNP compared to the BNP assay suggest that NT-proBNP could play an additional role in the evaluation of patients with LV systolic dysfunction.

Adult↗
PubMed2005

Preservation of renal function after heart transplantation: initial single-center experience with sirolimus.

BACKGROUND: Long-term survivors of heart transplantation are often confronted with chronic kidney disease, by definition related to the intake of calcineurin-inhibitors. Sirolimus is increasingly proposed as an alternative immunosuppressive agent due to its absence of nephrotoxicity. METHODS: Between November 2002 and November 2003, 9 adult heart transplant candidates with moderate to severe chronic renal disease were switched from cyclosporine to sirolimus. The conversion scheme consisted of an immediate stop of cyclosporine and an 8-mg loading dose of sirolimus, followed by 3 mg/d; after 1 week, the sirolimus dose was adjusted to maintain trough levels between 5 and 15 microg/L. The majority of patients were on corticosteroids, and on either azathioprine or mycophenolate mofetil. At conversion, the mean serum creatinine level was 2.11 (+/-0.4) mg/dL and the mean glomerular filtration rate (GFR) was 32 (+/-7) mL/min/1.73 m(2). Prior to conversion, the renal dysfunction was predominantly stable. RESULTS: After conversion, there were 7 dropouts (75%) due to several side effects related to sirolimus: edema (n = 2), general discomfort (n = 2), delayed wound healing (n = 1), cardiac thrombus (n = 1), and diarrhea (n = 1). The median treatment time with Sirolimus, therefore, was only 4.0 months. While on sirolimus, the renal function of all patients remained unchanged or showed even some improvement. Retrospective nephrological review revealed severe renal artery stenoses in 2 patients and serious generalized abdominal and renal atheromatosis in 7 patients. No cardiac dysfunction was seen. CONCLUSION: Conversion from cyclosporine to sirolimus was problematic due to sirolimus side effects, occurring at any time after the switch. One should also question whether chronic kidney disease after heart transplantation is routinely caused by the administration of calcineurin-inhibitors, in view of the generalized renal and abdominal atheromatosis.

Aged↗
PubMed2005

Myocardial cytokine gene expression is higher in aortic stenosis than in idiopathic dilated cardiomyopathy.

OBJECTIVE: To investigate cytokine gene expression in patients with aortic valve stenosis (AS) and with idiopathic dilated cardiomyopathy (DCM), and to correlate wall stress with myocardial proinflammatory cytokine gene expression. METHODS: Human left ventricular (LV) myocardial biopsies were obtained for subsequent reverse transcription polymerase chain reaction of tumour necrosis factor alpha (TNFalpha), interleukin (IL)-1beta, and IL-6 mRNA. The study population consisted of 24 patients with AS and 10 patients with idiopathic DCM. RESULTS: Patients with AS had a larger ejection fraction (56 (5) v 37 (4)%, p < 0.01), smaller LV end diastolic volumes (146 (11) v 267 (21) ml, p < 0.01), and lower end systolic wall stress (44 (7) v 112 (11) kdyn/cm2, p < 0.001). Upregulation of TNFalpha, IL-1beta, and IL-6 gene expression was detected in both groups. However, TNFalpha gene expression was significantly higher in AS than in DCM (p = 0.009). No correlation was found between haemodynamic parameters and TNFalpha gene expression. In patients with AS there was a strong inverse relation between circulating TNFalpha and TNFalpha gene expression (r = -0.685, p = 0.014), between circulating TNFalpha and IL-1beta gene expression (r = -0.664, p = 0.018), and between soluble TNF receptor 2 and TNFalpha gene expression (r = -0.685, p = 0.020). Myocardial gene expression of TNFalpha was significantly higher in patients with well compensated AS than in patients with decompensated AS (p = 0.017). Similarly, patients with decompensated DCM were characterised by significantly lower TNFalpha gene expression than were patients with well compensated DCM (p = 0.011). CONCLUSION: TNFalpha gene expression is significantly higher in patients with pressure overload than in normal hearts, in patients with idiopathic DCM, and in patients with compensated versus decompensated heart failure. Secondly, in patients with AS proinflammatory cytokine gene expression did not affect systolic performance. The higher TNFalpha gene expression in patients with compensated heart failure suggests that cytokine gene expression has an adaptive role in the early phase of LV remodelling.

Aged↗
PubMed2004

Acute type A aortic dissection in a cardiac allograft recipient: case report and review of the literature.

Dissection of the ascending aorta is uncommon in cardiac allograft recipients and usually affects the native aorta. The diagnosis is often made at necropsy. The first case is reported of a Bentall procedure performed in a heart transplant recipient who presented with ascending aortic dissection of the donor aorta and concomitant aortic regurgitation seven years after orthotopic transplantation.

Aged↗
PubMed2001

A synthetic factor-Xa inhibitor (ORG31540/SR9017A) as an adjunct to fibrinolysis in acute myocardial infarction. The PENTALYSE study.

BACKGROUND: ORG31540/SR90107A, a synthetic pentasaccharide, is a selective inhibitor of factor-Xa. It was hypothesized that prolonged factor-Xa inhibition with pentasaccharide may be an effective and safe antithrombotic co-therapy in acute myocardial infarction. METHODS AND RESULTS: Patients (n=333) with evolving ST-segment elevation acute myocardial infarction were treated with aspirin and alteplase and randomized to unfractionated heparin, given intravenously during 48 to 72 h, or to a low, medium or high dose of pentasaccharide, administered daily for 5 to 7 days, intravenously on the first day, then subcutaneously. Coronary angiography was performed at 90 min and on days 5 to 7. Thrombolysis in Myocardial Infarction (TIMI) flow grade 3 rates at 90 min were similar in the four treatment groups. Among patients with TIMI 3 flow at 90 min and who did not undergo a coronary intervention (n=155), a trend towards less reocclusion of the infarct-related vessel on days 5 to 7 was observed with pentasaccharide: 0.9% vs 7.0% with unfractionated heparin (P=0.065). Also, fewer revascularizations during the 30-day follow-up period were performed in patients given pentasaccharide (39% vs 51% for unfractionated heparin;P=0.054). The primary safety end-point, the combined incidence of intracranial haemorrhage and need for blood transfusion, was identical with pentasaccharide and unfractionated heparin (7.1%). One non-fatal intracranial haemorrhage occurred in the 241 patients given pentasaccharide (0.4%). CONCLUSIONS: In this study, pentasaccharide given together with alteplase was safe and as effective as unfractionated heparin in restoring coronary artery patency. Prolonged administration of pentasaccharide was associated with a trend towards less reocclusion and fewer revascularizations. Selective factor-Xa-inhibition seems to be an attractive therapeutic concept in patients presenting with ST-segment elevation acute myocardial infarction.

Adult↗
PubMed2001

Leiomyosarcoma of the right ventricle extending into the pulmonary trunk.

Primary leiomyosarcomas of the heart, particularly those affecting the right ventricle, are uncommon. A 70 year old woman presenting with the symptoms of progressive exertional dyspnoea and left sided pleuritic pain is presented. A leiomyosarcoma was diagnosed that originated in the right lateral ventricle wall, causing pulmonary outflow obstruction. Pathological analysis showed a neoplasm with a myxoid stroma, high mitotic activity, and nuclei expressing atypia. Immunohistochemical staining was found positive for vimentin and desmin. Seven months after complete surgical resection the tumour relapsed. This case illustrates the poor outcome, high relapse rate, and inefficiency of treatment associated with primary cardiac leiomyosarcomas. The current literature regarding incidence, diagnostic techniques, treatment strategies, and survival rates of this rare but terminal disease is reviewed.

Aged↗
PubMed2001

Ventricular outflow tract obstruction secondary to leiomyosarcoma of the right ventricle.

Primary leiomyosarcomas of the heart, particularly those affecting the right ventricle, are uncommon. We report the case of a 70-year-old Belgian woman presenting with the symptoms of progressive exertional dyspnea and left-sided pleuritic pain. A leiomyosarcoma which originated from the right lateral ventricle wall, causing pulmonary outflow obstruction, was diagnosed. Pathology revealed a neoplasm with a myxoid stroma, high mitotic activity and nuclei expressing atypia. Immunohistochemical staining was positive for vimentine and desmin. Seven months after complete surgical resection the tumor relapsed. This case demonstrates the poor outcome, the high relapse rate and inefficiency of treatment associated with primary cardiac leiomyosarcomas. The current literature regarding the incidence, diagnostic techniques, treatment strategies and survival rates of this rare but terminal disease is reviewed.

Aged↗
PubMed2001

Unstable angina due to spontaneous dissection of a LIMA graft.

We report a case of a spontaneous dissection of a left internal mammary artery grafted on the diagonal branch and the left anterior descendens. The clinical and diagnostic features of this condition are discussed. Despite an extensive literature search, no such case could be found. This case report must be regarded as the first. We speculate that extensive kinking of the left internal mammary artery contributed in the pathogenesis of this syndrome.

Angina, Unstable↗
PubMed1999

Endomyocardial nitric oxide synthase and left ventricular preload reserve in dilated cardiomyopathy.

BACKGROUND: Patients with heart failure have modified myocardial expression of nitric oxide synthase (NOS), as is evident from induction of calcium-insensitive NOS isoforms. The functional significance of this modified NOS gene expression for left ventricular (LV) contractile performance was investigated in patients with dilated nonischemic cardiomyopathy. METHODS AND RESULTS: In patients with dilated, nonischemic cardiomyopathy, invasive measures of LV contractile performance were derived from LV microtip pressure recordings and angiograms and correlated with intensity of gene expression of inducible (NOS2) and constitutive (NOS3) NOS isoforms in simultaneously procured LV endomyocardial biopsies (n=20). LV endomyocardial expression of NOS2 was linearly correlated with LV stroke volume (P=0.001; r=0.66), LV ejection fraction (P=0.007; r=0.58), and LV stroke work (P=0.003; r=0.62). In patients with elevated LV end-diastolic pressure (>16 mm Hg), a closer correlation was observed between endomyocardial expression of NOS2 and LV stroke volume (P=0.001; r=0.74), LV ejection fraction (P=0.0007; r=0.77), and LV stroke work (r=0.82; P=0.0002). LV endomyocardial expression of NOS3 was linearly correlated with LV stroke volume (P=0.01; r=0.53) and LV stroke work (P=0.01; r=0.52). To establish the role of nitric oxide (NO) as a mediator of the observed correlations, substance P (which causes endothelial release of NO) was infused intracoronarily (n=12). In patients with elevated LV end-diastolic pressure, an intracoronary infusion of substance P increased LV stroke volume from 72+/-13 to 91+/-16 mL (P=0.06) and LV stroke work from 67+/-11 to 90+/-15 g. m (P=0.03) and shifted the LV end-diastolic pressure-volume relation to the right. CONCLUSIONS: In patients with dilated cardiomyopathy, an increase in endomyocardial NOS2 or NOS3 gene expression augments LV stroke volume and LV stroke work because of a NO-mediated rightward shift of the diastolic LV pressure-volume relation and a concomitant increase in LV preload reserve.

Adult↗
PubMed1999

ECG diagnosis of native heart ventricular tachycardia in a heterotopic heart transplant recipient.

A case is reported of haemodynamic collapse in a 51 year old male heterotopic heart transplant recipient caused by native heart ventricular tachycardia. An accurate diagnosis was made by selective right and left sided electrocardiography. Synchronised electrical cardioversion of the native heart (200 J) resulted in restoration of sinus rhythm with prompt relief of symptoms and amelioration of the clinical situation.

Electric Countershock↗
PubMed1999

Pacing in cardiomyopathy.

Permanent cardiac pacing is an established treatment for the prevention of syncope or sudden death in patients with heart block or sinus node disease. Recent observations underscore the use of pacing in patients with various forms of cardiomyopathy, i.e. hypertrophic, dilated and tachycardia-induced cardiomyopathy. The evidence favouring the use of pacing in patients with cardiomyopathy is mainly derived from retrospective and uncontrolled investigations and the data from the scarce randomized investigations are rather disappointing. Therefore, the indications for pacing remain controversial.

Belgium↗
PubMed1998

Different humoral responses during head-up tilt testing among patients with neurocardiogenic syncope.

Neurocardiogenic dysfunction is believed to result from activation of ventricular mechanoreceptors. To asses other humoral and circulatory mechanisms activated during vasovagal syncope, epinephrine, norepinephrine, renin, and aldosterone levels were measured during head-up tilt testing. Twenty-three patients referred because of vasovagal syncope underwent passive head-up tilt testing (80 degrees). Blood samples were taken at baseline, after 30 minutes of supine rest and at syncope. Five patients (four men, one woman; mean age 46 +/- 27 years) had cardioinhibitory syncope. Seven patients (five men, two women; mean age 40 +/- 12 years) had vasodepressor syncope. Eleven patients (eight men, three women; mean age 55 +/- 21 years) had negative results of head-up tilt tests. Among patients with cardioinhibitory syncope, norepinephrine concentration rose significantly from baseline to syncope (0.44 +/- 0.12 ng/ml versus 1.14 +/- 0.72 ng/ml; p < 0.05), whereas no significant change was observed in epinephrine (0.08 +/- 0.03 ng/ml versus 2.74 +/- 2.85 ng/ml; p = not significant [NS]), renin (5.68 +/- 3.03 pg/ml versus 19.58 +/- 11.47 pg/ml; p = NS), or aldosterone concentration (66.60 +/- 16.10 ng/ml versus 109.00 +/- 44.70 ng/ml; p = NS). Patients with vasodepressor syncope had a significant rise in renin (9.03 +/- 4.56 pg/ml versus 52.53 +/- 41.63 pg/ml; p < 0.05) and aldosterone concentration (95.43 +/- 103.03 ng/ml versus 249.57 +/- 191.54 ng/ml; p < 0.05), whereas no change in level of epinephrine (0.12 +/- 0.12 ng/ml versus 0.28 +/- 0.33 ng/ml; p = NS) or norepinephrine (0.60 +/- 0.26 ng/ml versus 0.86 +/- 0.53 ng/ml; p = NS) was detected. Among patients with negative results of tilt tests, levels of renin (7.94 +/- 7.19 pg/ml versus 27.71 +/- 18.50 pg/ml; p < 0.01) and aldosterone (64.64 +/- 28.33 ng/ml versus 160.91 +/- 79.58 ng/ml; p < 0.01) rose significantly, whereas no change was seen in epinephrine (0.12 +/- 0.14 ng/ml versus 0.23 +/- 0.31; p = NS) or norepinephrine concentration (0.54 +/- 0.21 ng/ml versus 0.82 +/- 0.52; p = NS). Patients with cardioinhibitory syncope were characterized by a rise in norepinephrine level and blunted activation of the renin-angiotensin-aldosterone axis at syncope. Unlike patients with cardioinhibitory syncope, the renin-angiotensin-aldosterone axis is activated in patients with vasodepressor syncope and patients with a negative result of head-up tilt test without a statistically significant increase in catecholamine levels. Patients with cardioinhibitory syncope have higher epinephrine levels at syncope compared with patients with a negative result of head-up tilt test and patients with vasodepressor syncope.

Adult↗
PubMed1998

Pro-inflammatory cytokines and endothelium-dependent vasodilation in the forearm. Serial assessment in patients with congestive heart failure.

BACKGROUND: In patients with heart failure endothelium-dependent vasodilation of the forearm conduit vessels is impaired possibly because of elevated plasma levels of pro-inflammatory cytokines. The effect of elevated plasma cytokines on endothelium-dependent vasodilation of forearm conduit vessels was therefore serially investigated in 16 patients with congestive heart failure during an episode of acute failure and at the time of recompensation. METHODS AND RESULTS: Pro-inflammatory cytokine levels and hyperaemic brachial artery diameters were obtained shortly after admission for an episode of acute heart failure and 11 +/- 3 days later at the time of recompensation, which was obtained using diuretic therapy without changing other cardiovascular medications. Serum concentrations (Mean +/- SD) of tumour necrosis factor alpha (TNF-alpha) (decompensation vs recompensation: 25 +/- 23 pg.ml-1 vs 26 +/- 17 pg.ml-1) and interleukine 6 (IL-6) (decompensation vs recompensation: 27 +/- 24 pg.ml-1 vs 20 +/- 18 pg.ml-1), determined in venous blood using immunoradiometric assays were elevated but remained unaltered following recompensation. Brachial artery diameter, derived from high-resolution ultrasound scans at rest and during reactive hyperaemia, 90 s after forearm cuff deflation, increased significantly during reactive hyperaemia at the time of admission (3.4 +/- 0.7 mm vs 4.0 +/- 0.5 mm; P = 0.014) and following recompensation (3.4 +/- 0.5 mm vs 3.8 +/- 0.2 mm; P = 0.032). The brachial artery diameter during recompensation expressed as a percentage of the baseline value was similar at both intervals (decompensation vs recompensation: 117 +/- 14% vs 116 +/- 10%; P = ns). At the time of decompensation, the correlation between TNF-alpha and the percentage change in brachial artery diameter following reactive hyperaemia was absent (r = 0.098; P = 0.719). The same correlation became significant at the time of recompensation (r = 0.750; P = 0.001). CONCLUSIONS: In patients with congestive heart failure, plasma levels of pro-inflammatory cytokines correlate with endothelium-dependent vasodilation of the brachial artery following recompensation, but not during an acute episode of heart failure.

Acute Disease↗
PubMed1998

Early benefit of implantable cardioverter defibrillator therapy in patients waiting for cardiac transplantation.

The ICD can effectively recognize and treat ventricular arrhythmias that can lead to sudden death. Sudden death is a major problem in patients awaiting heart transplantation. We reviewed our experience with the ICD in patients with malignant ventricular arrhythmias waiting for cardiac transplantation. Nineteen patients were included. Seventeen were men, mean age was 54 +/- 11 years (range 17-66) and the left ventricular ejection fraction was 22% +/- 10% (range 9%-46%). After a mean follow-up of 6 +/- 5 months (range 1-20 months), 17 patients reached heart transplantation. One patient died and the other is waiting for a transplant. Before transplantation 71% of patients received an appropriate discharge. The mean time to the first appropriate discharge was 2 +/- 2 months (range < 1-6 months), which was significantly shorter than the mean time to first discharge in the other patients (n = 182) receiving a defibrillator in our center (11 +/- 10 months; range 1-58 months) (P < 0.0004). In conclusion, cardiac transplantation candidates with life-threatening ventricular arrhythmias can effectively be protected against sudden arrhythmic death by ICD. These patients have a high incidence of appropriate shocks occurring very early after implantation.

Adolescent↗