Biomedical subjects
Publications and source records attributed to M Vanderheyden.
We describe a patient with hemodynamic deterioration and worsening mitral regurgitation related to right ventricular apex pacing. Time-dependent changes in papillary muscle contraction as well as ventricular remodeling by right ventricular apex pacing might be responsible for this rare but serious complication.
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Thrombotic thrombocytopenic purpura (TTP) is a known, although rare, complication of ticlopidine treatment. It typically appears within the first days or weeks after initiation of therapy. We describe a case of TTP in a 75-year-old patient, due to ticlopidine, occurring three weeks after coronary stent implantation. The patient responded favourably to fresh frozen plasma exchanges. We are reporting this case to emphasize that prognosis depends on prompt diagnosis and early treatment, implying careful biochemical monitoring.
BACKGROUND: Myocardial expression of inducible (i) nitric oxide (NO) synthase (iNOS) gene has been reported in transplant recipients and in dilated cardiomyopathy. NO derived from NO donor or from coronary endothelium has previously been shown in the human heart to reduce end-systolic left ventricular (LV) pressure, especially during beta-adrenoreceptor stimulation, because of earlier onset of LV relaxation. The present study investigated in transplant recipients whether a similar cardiodepressant effect could be attributed to NO derived from iNOS. METHODS AND RESULTS: In 16 transplant recipients who were free of rejection or graft vasculopathy, microtip LV pressure recordings, LV angiograms, and endomyocardial biopsies were obtained at annual coronary angiography. In 8 transplant recipients, microtip LV pressure recordings were obtained during intravenous dobutamine (5 microg x kg(-1) x min(-1)). Competitive reverse transcription-polymerase chain reaction of iNOS mRNA was performed on the endomyocardial biopsies, and the intensity of iNOS mRNA expression was quantified on a scale ranging from 0 to 5+. All measures of baseline LV function were comparable in transplant recipients with low (< or = 2+) or high myocardial iNOS mRNA. During intravenous dobutamine infusion, there was a significant correlation between the abbreviation of LV electromechanical systole time (LVEST is the time from onset of QRS to dP/dt(min)) and the rise of LV dP/dt(max) (r=.79; P<.02). By use of a multiple regression analysis, addition of the intensity of iNOS mRNA expression as an independent variable significantly (P<.005) improved the correlation between deltaLVEST and deltaLV dP/dt(max) (P<.001; r=.97), implying a larger abbreviation of LV contraction for a similar rise in LV dP/dt(max), when myocardial iNOS mRNA was higher. The larger abbreviation of LV contraction in-patients with high iNOS mRNA was associated with a decrease in LV end-systolic pressure (-31+/-16 mm Hg). CONCLUSIONS: Myocardial iNOS gene expression in the human allograft influences the LV contractile response to beta-adrenergic stimulation through earlier onset of LV relaxation and reduction of LV end-systolic pressure. These effects are similar to the LV contractile effects of NO derived from NO donor or from coronary endothelium.
BACKGROUND: In humans, intracoronary infusion of substance P reduces left ventricular end-systolic pressure and left ventricular peak systolic pressure because of earlier onset of left ventricular relaxation induced by paracrine myocardial action of mediators released from the coronary endothelium. The present study investigated in humans the effects of beta-adrenergic stimulation, which also induces earlier left ventricular relaxation, on the left ventricular myocardial contractile response to intracoronary infusion of substance P. METHODS AND RESULTS: Data were obtained in 13 patients after cardiac transplantation and in 3 patients with dilated nonischemic cardiomyopathy. Microtip left ventricular pressure recordings were obtained during a 5-minute intracoronary infusion of substance P (20 pmol/min) under control conditions and then repeated during concurrent intravenous administration of dobutamine. In the presence of dobutamine, intracoronary substance P caused a greater fall in left ventricular end-systolic pressure (transplantation control, -9 +/- 11 versus transplantation dobutamine, -20 +/- 18 mm Hg [P < .05]; cardiomyopathy control, -4 +/- 1 versus cardiomyopathy dobutamine, -10 +/- 3 mm Hg [P < .05]) and in left ventricular peak systolic pressure (transplantation control, -14 +/- 10 versus transplantation dobutamine, -30 +/- 22 mm Hg [P < .01]; cardiomyopathy control, -9 +/- 7 versus cardiomyopathy dobutamine, -15 +/- 6 mm Hg [P = .1]). CONCLUSIONS: Dobutamine enhances the cardiodepressant effect on myocardial contractile performance of receptor-mediated coronary endothelial stimulation in transplant recipients and in patients with dilated nonischemic cardiomyopathy. This enhancement could result from a potentiating interaction of the relaxation-hastening effect exerted by beta-adrenergic stimulation and by mediators released from the coronary endothelium, such as nitric oxide.
OBJECTIVES: In the present study, we investigated, in transplant recipients, whether L-arginine (L-arg) potentiates the myocardial contractile effects of receptor-mediated coronary endothelial stimulation. Moreover, because inducible nitric oxide synthase (iNOS) is frequently expressed in transplanted myocardium, we also performed intracoronary infusion of L-arg in the absence of receptor-mediated coronary endothelial stimulation to investigate whether similar left ventricular (LV) contractile effects could be induced by providing more substrate for iNOS. BACKGROUND: Nitric oxide (NO), released from coronary endothelium after receptor-mediated stimulation by substance P (SP), affects vascular smooth muscle tone and modulates LV contractile performance. L-arg augments receptor-mediated endothelium-dependent coronary vasodilation in transplant recipients by increasing substrate availability for endothelial NO production. METHODS: Sixteen transplant recipients were studied at the time of annual coronary angiography. In eight transplant recipients, microtip LV pressures were recorded before and during intracoronary (IC) SP (20 pmol/min) and after the addition of IC L-arg (160 mumol/min) to IC SP. In eight transplant recipients, microtip LV pressures were recorded before and during IC L-arg (160 mumol/min) alone, and in six of these patients, endomyocardial biopsy samples were obtained to detect the expression of iNOS gene by reverse transcription-polymerase chain reaction. RESULTS: Addition of IC L-arg to IC SP induced a fall (mean +/- SEM) in LV peak systolic pressure (-16 +/- 4 mm Hg), which was larger (p < 0.01) than that observed during IC SP (-7 +/- 2 mm Hg). During IC L-arg alone, there was no change in LV peak systolic pressure despite the presence of iNOS mRNA in five of the six biopsy samples. CONCLUSIONS: In transplant recipients, L-arg potentiates the paracrine myocardial contractile effects of receptor-mediated coronary endothelial stimulation, probably by providing more substrate for endothelial NO production. Despite the myocardial expression of iNOS gene, L-arg alone fails to elicit similar contractile effects.
Radiofrequency ablation of the atrioventricular conduction system (ACS) has become an established therapy for patients with drug refractory atrial fibrillation. We observed eight patients with hemodynamic deterioration after radiofrequency ablation of the atrioventricular conduction system. As we found hemodynamic deterioration related to worsening mitral regurgitation, we compared the clinical history, electrophysiological, and echocardiographic data from the patients with hemodynamic deterioration and worsening mitral regurgitation (group 1) to those without hemodynamic deterioration and stable mitral regurgitation after the procedure (group 2). Eight out of 108 patients (7.4%) undergoing ablation of the ACS deteriorated hemodynamically with acute pulmonary edema in three and congestive heart failure in five patients occurring at a mean of 3 and 8 weeks, respectively, after the procedure. Three of these patients were referred for mitral valve surgery. Two patients underwent ablation using a left-sided approach. A right-sided approach was used in five patients. In one patient, a left- and right-sided approach was used. Compared to group 2 patients, group 1 patients had significantly higher left ventricular end-diastolic diameters (64 +/- 6 mm vs 56 +/- 9 mm) at baseline despite similar fractional shortening (32% +/- 11% vs 34% +/- 13%), left ventricular end-systolic diameters (43 +/- 9 mm vs 36 +/- 7 mm) and degree of mitral regurgitation (1.4 +/- 1.1 vs 1.4 +/- 0.7) on echocardiographic analysis. Thus, hemodynamic deterioration together with progression of mitral regurgitation is a potential complication of ablation of the ACS (up to 7.4%). Patients with high left ventricular end-diastolic diameters and moderate mitral regurgitation at baseline seem prone to this complication.
Partial congenital absence of the left pericardium is a rare abnormality which may provoke serious complications. We report the case of a young adult, suffering from chest pain due to incarceration of atrial tissue. Based on this case report the clinical, pathophysiological and diagnostic features of this condition are described.
The search for a pacemaker that accurately and easily mimics normal physiology is a continuing effort. Present pacing developments include AV synchrony and rate adaptiveness. The usefulness and clinical value of some of the new pacing systems remain unclear. Although the hemodynamic advantages of rate responsive pacing over classical ventricular pacing are well established (Kristensson et al., 1985), an ideal sensor for physiological demands has not been established. We report a case of apparently unequivocal increase in heart rate during upper limb movements in a patient with a VVI-R pacemaker using minute ventilation as a sensor. Inappropriate heart rate acceleration may result from changes in transthoracic impedance due to upper limb exercise and it does not necessarily represent sensor malfunction. Although this complication is well-known in VVI-R pacemakers using respiratory rate or minute ventilation as sensor (Santomauro et al., 1992), one must remain aware of this sensor-related problem. In this particular patient the problem could be solved by implanting the pacemaker can more medially.
This study describes a dynamic left ventricular outflow tract gradient complicating an acute anterior myocardial infarction in two patients. In both cases, hyperdynamic contraction of the non-infarcted segments were noted in addition to large antero-apical a- or dyskinesia. Both patients had evidence of mitral annular calcifications, and the occurrence of dynamic outflow tract obstruction preceded sudden death. Early recognition of the underlying pathophysiological mechanism might have major therapeutic implications and could decrease the risk of myocardial rupture.
An inflammatory pseudotumour of the lung in an achondroplastic woman is described. The occurrence of both conditions in the same patient probably represents a coincidental finding. However, recurrent pulmonary infections, as frequently seen in achondroplasia, may be relevant, because a history of antecedent infection is noted in one third of cases of inflammatory pseudotumours. Despite extensive debridement of the pseudotumour by neodymium yttrium aluminium garnet (NdYAG) laser therapy, early recurrence occurred.
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