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Marc Vanderheyden

Publications and source records attributed to Marc Vanderheyden.

32 records · Page 2Linked to original sources

Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy.

OBJECTIVES: We postulated that both diastolic and systolic load modulate B-type natriuretic peptide (BNP) production in human pressure overload hypertrophy/failure. BACKGROUND: In isolated myocytes, diastolic stretch induces BNP messenger ribonucleic acid expression. However, the mechanism of the BNP release in human hypertrophy remains controversial. METHODS: In 40 patients with symptomatic aortic stenosis (AS), left ventricular (LV) performance and systolic and diastolic wall stress were calculated from combined invasive and echocardiographic data. Plasma BNP was determined by the rapid point-of-care bedside analyzer (Biosite Triage, Biosite Diagnostics Inc., San Diego, California). RESULTS: A significant relationship was observed between plasma BNP and pulmonary capillary wedge pressure (p < 0.001), fractional shortening (p = 0.001), and aortic valve area (p = 0.006). Furthermore, a significant correlation was noted between BNP and LV mass index (p = 0.005) as well as between BNP and markers of diastolic load such as LV end-diastolic wall stress (p = 0.011), indexed LV end-diastolic volume (p < 0.001), and isovolumic relaxation time (p = 0.02). Preoperative BNP levels were elevated in patients with AS compared with patients without AS. Plasma BNP was higher in AS patients with impaired versus normal preload reserve (297 +/- 56 pg/ml vs. 168 +/- 44 pg/ml; p = 0.017) and in AS patients with clinical deterioration after valve replacement compared with those without (399 +/- 82 pg/ml vs. 124 +/- 41 pg/ml; p = 0.011). CONCLUSIONS: In patients with AS, BNP appears to be regulated not only by systolic but also by diastolic load. This supports the hypothesis that myocardial stretch modulates BNP production in human pressure overload hypertrophy/failure.

Adult↗

Brain and other natriuretic peptides: molecular aspects.

Natriuretic peptides have emerged as important candidates for development of diagnostic tools and therapeutic agents in cardiovascular disease. The family contains of three major peptides-ANP, BNP, CNP-that participate in cardiovascular and cardiorenal homeostasis. Each of these natriuretic peptides binds differentially to specific receptors that signal through different mechanisms. They are cleared enzymatically by neutral endopeptidase as well as by receptor-mediated endocytosis. Because of its fast induction and specific expression in overt heart failure, BNP seems the most promising natriuretic peptide. It is predominantly synthesized in the cardiac ventricles, released as pre-proBNP and then enzymatically cleaved to BNP and the N-terminal portion of BNP(NT-proBNP). Blood measurements of BNP and NT-proBNP have been shown to identify patients with LV dysfunction. This review focuses on the physiology of natriuretic peptides as a group and brain natriuretic peptide in more detail, its structure and regulation as well as its effects at the cellular level.

Atrial Natriuretic Factor↗

Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography.

BACKGROUND: Cardiac resynchronization therapy was shown to reverse left ventricular (LV) remodeling in patients with congestive heart failure (CHF). However, the prediction of benefit is controversial. We aimed to investigate predictive factors of LV functional recovery and reversed remodeling after biventricular pacing. METHODS AND RESULTS: Forty-nine consecutive patients with CHF and a wide QRS complex (182+/-32 ms) were studied by echocardiography before resynchronization. Intraventricular and interventricular asynchrony and their combination were assessed by pulsed-wave tissue Doppler imaging from measurements of regional electromechanical coupling times in basal segments of the right and left ventricle. At 6-month follow-up, responders were defined by a relative increase in LV ejection fraction > or =25% compared with baseline (n=27). Receiver operating curve analysis revealed the degree of intraventricular asynchrony (area under the curve=0.77), interventricular asynchrony (area under the curve=0.69), and their combination (area under the curve=0.84) as the best predictors of functional recovery after resynchronization. In addition, the degree of intraventricular and interventricular asynchrony correlated significantly with the improvement of LV ejection fraction (r=0.73, P<0.0001), end-diastolic diameter (r=-0.59, P<0.0001), and end-systolic diameter (r=-0.48, P<0.001) at follow-up. QRS duration and conventional echo-Doppler indices were not predictive of reversed LV remodeling. CONCLUSIONS: In patients with CHF, the degree of intraventricular and interventricular asynchrony and their combination are the best predictive factors of LV functional recovery and reversed remodeling after cardiac resynchronization therapy.

Aged↗

Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses.

BACKGROUND: Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced alpha-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia. AIM: To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine. METHODS AND RESULTS: Fractional flow reserve (FFR, calculated by coronary pressure measurements during adenosine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis (mean diameter stenosis of 50+/-1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an alpha1-, alpha2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective alpha1-adrenergic blocker; (c) 20 patients before and after IC bolus of saline. Since minimal luminal diameter remained unchanged before and after phentolamine (1.46+/-0.06 vs. 1.47+/-0.06 mm, ns), urapidil (1.46+/-0.06 vs. 1.39+/-0.08, ns), and saline (1.56+/-0.08 vs. 1.55+/-0.08, ns), changes in FFR reflects changes in microvascular resistance. Overall, phentolamine and urapidil induced a slight but significant decrease in FFR (phentolamine: 0.79+/-0.02 vs. 0.77+/-0.02, p<0.05; urapidil: 0.78+/-0.02 vs. 0.75+/-0.02, p<0.05). However, only 6 patients showed a change in FFR from > or = 0.75 to <0.75 and no patients showed a change in FFR from > or = 0.80 to <0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure. CONCLUSIONS: The administration of alpha-adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values do not significantly affect clinical decision making.

Adrenergic alpha-Antagonists↗

Hemodynamic effects of inducible nitric oxide synthase and nitrotyrosine generation in heart failure.

OBJECTIVES: The hemodynamic effects of cardiac inducible nitric oxide synthase (iNOS) and of iNOS-mediated peroxynitrite in patients with left ventricular (LV) dysfunction are unclear. The present study investigates the incidence and functional significance of iNOS expression and nitrotyrosine formation in patients with heart failure. METHODS: LV endomyocardial biopsies obtained from 24 patients with heart failure due to idiopathic dilated cardiomyopathy (ejection fraction [EF] <45% and left ventricular end-diastolic volume index [LVEDVI] >102 ml/m2) were analyzed for iNOS and nitrotyrosine. LV contractile performance was assessed by left ventricular ejection fraction (LVEF) and stroke work normalized for end-diastolic pressure (SW/EDP). LV filling pattern was assessed by Doppler E/A wave ratio, deceleration time (DT) of early LV filling and indexed LV end-diastolic volume normalized for EDP as a marker of diastolic distensibility. RESULTS: iNOS immunostaining correlated significantly with nitrotyrosine formation (r = 0.86, p < 0.001). In the whole study group, patients expressing iNOS (n = 13) showed larger LV end-diastolic (173 +/-16 vs 128 +/- 9 ml/m2, p = 0.031) and end-systolic volume indices (110 +/- 16 vs 61 +/- 9 ml/m2, p = 0.018) and similar LVEDP (18 +/- 2 vs 21 +/- 2 mm Hg, p = 0.227). In patients with advanced heart failure and reduced pre-load reserve (LVEDP > 16 mm Hg, n = 18), iNOS protein and nitrotyrosine formation correlated positively with LVSW/EDP (r = 0.65, p = 0.03 and r = 0.64, p = 0.04, respectively), DT (r = 0.96, p < 0.01 and r = 0.88, p < 0.01, respectively) and inversely with E/A (r = -0.82, p < 0.01 and r = -0.88, p < 0.01, respectively). In addition, nitrotyrosine formation correlated positively with LVEDVI/EDP (r = 0.64, p = 0.02). Advanced iNOS-positive heart failure patients had a higher LVEDVI/EDP compared with iNOS-negative patients (5.30 +/- 0.64 vs 3.13 +/- 0.34 ml/mm Hg x m2, p = 0.02). CONCLUSIONS: In heart failure, iNOS protein expression is associated with nitrotyrosine formation. Although iNOS-positive patients are generally characterized by larger LV volume and depressed function, the preserved NO generation appears to be associated with higher cardiac work due to the preserved Frank-Starling relationship in end-stage heart failure.

Adult↗

Ischemic cardiomyopathy: value of different MRI techniques for prediction of functional recovery after revascularization.

OBJECTIVE: The purpose of this study was to compare the value of different MRI techniques for the assessment of myocardial viability. SUBJECTS AND METHODS. Eighteen infarct patients (mean age +/- SD, 62 +/- 8 years) with myocardial ischemia were examined using MRI before and after revascularization. The MRI study before treatment consisted of an evaluation of first-pass perfusion, contractile function at rest and during dobutamine stress, and delayed hyperenhancement. Findings were correlated with segmental and global cardiac function after revascularization. RESULTS: In initially dysfunctional segments, the likelihood of functional recovery after revascularization was 91% for segments without delayed hyperenhancement, 43% for segments with delayed hyperenhancement with transmural extent of 75% or less, and 8% for segments with delayed hyperenhancement with transmural extent of more than 75% (p < 0.05). Improved function at dobutamine stress MRI indicated functional recovery in 87%, whereas functional recovery was observed in only 30% of segments not responding at dobutamine stress MRI (p < 0.05). No significant correlation was found between the results of first-pass perfusion MRI and functional recovery. The ejection fraction after revascularization was best predicted by the MRI-derived infarct volume (p < 0.001, R(2) = 0.63). CONCLUSION: A simple protocol consisting of baseline contractility and delayed enhancement MRI studies is adequate to differentiate dysfunctional but viable from nonviable myocardium. Dobutamine stress and perfusion MRI studies offer little or no additional information.

Aged↗

Deoxyribonucleic acid damage/repair proteins are elevated in the failing human myocardium due to idiopathic dilated cardiomyopathy.

OBJECTIVES: The study investigated the expression and relationship of deoxyribonucleic acid (DNA) repair enzymes with hemodynamic and nitric oxide (NO)-mediated stress in the failing myocardium. BACKGROUND: The role of apoptosis in human heart failure is controversial. Experimental studies suggested that NO-mediated stress modulates apoptosis of the cardiac myocytes. Of note, DNA repair enzymes such as redox factor/apurinic/apyridimine endonuclease Ref-1 protein, proliferative cell nuclear antigen (PCNA), the poly (ADP-ribose) polymerase (PARP), and DNA-protein kinase (DNA-PK) determine the cell fate after the DNA damage. METHODS: Left ventricular (LV) endomyocardial biopsies from 23 patients with dilated cardiomyopathy were analyzed by immunohistochemistry. RESULTS: Terminal deoxynucleotidyltransferase-mediated biotin-dUTP nick-end labeling (TUNEL) or cleaved caspase-3 and cleaved PARP could not be detected. The number of Ref-1-positive myocytes tended to be higher in patients with LV ejection fraction (EF) < or =35% versus LV EF >35% (21.23 +/- 4.8% vs. 13.8 +/- 5.8%, p = 0.1). The PCNA (7.1 +/- 2.8% vs. 0.9 +/- 0.6%, p = 0.05) and DNA-PK expressions (39.5 +/- 5.4% vs. 8.6 +/- 5.5%, p < 0.01) were higher in patients with LVEF < or =35% vs. LVEF >35%. The PCNA, Ref-1, and DNA-PK expression correlated with the LV end-systolic wall stress (r = 0.61, p < 0.01; r = 0.52, p < 0.01; and r = 0.73, p < 0.001, respectively). In addition, the PCNA and DNA-PK expression correlated with inducible NO synthase (r = 0.41, p = 0.05, and r = 0.53, p < 0.01, respectively). CONCLUSION: In this study, apoptosis could not be detected in the failing myocardium owing to idiopathic dilated cardiomyopathy. In contrast, failing myocardium was characterized by active DNA repair that was associated with elevated LV wall stress and activation of the inducible NO synthase.

Adult↗

Thrombosis of a patent foramen ovale closure device: thrombolytic management.

Transcatheter closure of a patent foramen ovale (PFO) offers a valuable alternative to surgery in selected patients with presumed paradoxical embolism. Like for all other devices, several complications have been described. Although the majority of these complications are caused by technical problems of the device itself, thrombosis is a relatively infrequent but feared finding, as it may result in recurrent embolic events and persistent neurological deficits. The majority of the complications after implantation are dealt with by surgical removal of the device and subsequent surgical closure of the PFO. The present case report describes biatrial thrombosis of a PFO device that was successfully treated with thrombolytics and GP IIb/IIIa receptor blockers. In stable patients, this pharmaco-therapeutic approach should be attempted to save the thrombosed PFO device and could therefore offer a valuable alternative to surgical removal of the device.

Echocardiography, Transesophageal↗

Intoxication with taxus baccata: cardiac arrhythmias following yew leaves ingestion.

The use of yew leaves (Taxus Baccata) as a means of deliberate self-harm is infrequent. The potent effect of the toxin is primarily cardiac and results in rhythm alterations and ultimately ventricular fibrillation. As there is no known antidote, and classic antiarrhythmic therapy proves to be ineffective, a prompt diagnosis is of great importance as immediate supportive action is the only valuable alternative. This case describes a 43-year-old women who attempted suicide by ingesting the leaves of Taxus Baccata. We discuss the effects and the difficulty of treatment associated with yew leaf poisoning.

Adult↗

Biventricular pacing and persistent left superior vena cava. Case report and review of the literature.

Persistent left superior vena cava is usually asymptomatic and does not cause any physiological problems (1). However it can severely complicate pacemaker implantation and render it sometimes impossible (2). In this case report we describe the implantation of a biventricular pacemaker using a left-sided approach in a patient with persistent left superior vena cava syndrome. A biventricular resynchronization device was used because of the reported beneficial haemodynamic effects of this pacing mode in patients with severe heart failure (3).

Aged↗

Symptomatic atraumatic dissection of a left internal mammary artery graft five years after coronary artery bypass graft surgery.

The case of a spontaneous dissection of a left internal mammary artery grafted on to the diagonal branch and the left anterior descending artery is reported. The clinical and diagnostic features of this condition are discussed. Despite an extensive literature search, no such case was found. The present case is the first to be reported. It was speculated that extensive kinking of the left internal mammary artery contributed to the pathogenesis of this syndrome.

Angioplasty, Balloon, Coronary↗