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Biomedical subjects

M Vrolix

Publications and source records attributed to M Vrolix.

35 records · Page 2Linked to original sources
PubMed1992

Specific coronary hemodynamic effects of nisoldipine and other vasoactive drugs.

The specific coronary hemodynamic effects of different vasoactive drugs were studied using a randomized, double-blind protocol in the "normal" contralateral artery after performing single-vessel coronary angioplasty. The intracoronary administration of 50 micrograms of nisoldipine resulted in an increase in epicardial diameter (+19%; p = 0.0001) and in coronary blood flow (+47%; p = 0.003), but the flow reserve decreased (-20%; p = 0.001). In placebo-treated patients, all parameters proved to be very stable and no significant changes were found. In a second study, 500 micrograms of diltiazem i.c. was administered to 20 patients, who were first randomized to pretreatment with either placebo (n = 10) or isosorbide dinitrate (0.5 micrograms/kg/min infusion; n = 10). There were increases in epicardial diameter (+10%; p = 0.0001) and coronary flow (+30%; p = 0.0001) in all patients. These changes were comparable in patients pretreated with placebo or nitrates but the reduction in coronary flow reserve was only significant in patients pretreated with placebo (+19%; p = 0.0008). In a third study, the hemodynamic effects of the intracoronary application of SIN-1 (500 micrograms), the active metabolite of molsidomine, were studied. There was a consistent increase in epicardial diameter (+26%; p < 0.0001) but the response at the microvascular level was heterogeneous and characterized by a trend to increased blood flow (+25%; p = 0.11) and decreased coronary vascular resistance (-18%; p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1991

Ridogrel in the setting of percutaneous transluminal coronary angioplasty.

The safety of the combination of heparin and ridogrel therapy and its antiplatelet efficacy was examined in the setting of percutaneous transluminal coronary angioplasty (PTCA). In 32 patients without known aspirin intake for 10 days before PTCA, therapy with ridogrel (300-mg intravenous bolus) was begun just before PTCA and continued orally at a dose of 300 mg twice daily until discharge. Heparin was administered as a 10,000 IU bolus dose before PTCA and followed by an intravenous infusion at a rate of 1,000 IU/hour for 24 hours. Bleeding problems at the arterial entry site occurred in 13 patients, which required a blood transfusion in only 2 patients. One patient underwent emergency bypass surgery without specific problems of hemostasis. Ridogrel virtually eliminated thromboxane B2 from the serum (29,990 +/- 6,555 pg/0.1 ml before vs 63 +/- 7 pg/0.1 ml at 2 hours after ridogrel), with a concomitant increase in serum 6-keto-prostaglandin F1 alpha (511 +/- 34 pg/0.1 ml before vs 1,190 +/- 146 pg/0.1 ml at 24 hours after ridogrel). There were no acute reocclusions in the ridogrel-treated patients, whereas acute reocclusions occurred in 5.6% of the patients taking the standard aspirin + heparin regimen during the same period. Furthermore, at 6-month clinical follow-up patients treated with ridogrel compared favorably with those receiving standard treatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Immediate and short-term results of a 1988-1989 coronary angioplasty registry.

To determine the relevance of recent refinements in angioplasty technology to our particular practice, the records of 507 consecutive patients undergoing a first percutaneous transluminal coronary angioplasty (PTCA) at our center between October 1988 and May 1989 were reviewed. At the time of PTCA, 41% of these patients had class IV angina and 44% were identified as having multivessel disease. Dilatation was attempted in 734 lesions (mean 1.5 per patient), of which 95 (13%) were chronic total occlusions. Overall, 69% of the 734 lesions were judged anatomically complex, and, in dilating these lesions, a rail-type device was used almost exclusively. Successful dilatation was achieved in 659 of the 734 (90%) attempted lesions. There were low incidences of the major complications of death (0.4%), myocardial infarction (1.8%) and emergency bypass surgery (1.8%). Acute rethrombosis occurred in 54 patients (11%). In these patients, initial strategy of repeat dilatation was successful in 38 of 47 patients (81%). Overall, primary clinical success at PTCA was achieved in 480 patients (95%). At a mean follow-up of 7.5 +/- 1.5 months in 497 of the study patients, the event-free rate (freedom from cardiac death, myocardial infarction, repeat PTCA or coronary bypass surgery or recurrence of severe [class III to IV] angina) was 71%. In conclusion, despite the often complex coronary disease in patients currently presenting to our center, a high initial success rate and acceptable short-term outcome of PTCA was achieved.

Aged↗
PubMed1991

Lack of evidence for small vessel disease in a patient with "slow dye progression" in the coronary arteries.

A patient with chest pain of recent onset, suggestive for angina pectoris, was referred for diagnostic coronary angiography, which showed the typical phenomenon of "slow dye progression" in the absence of any significant coronary artery stenosis. While intracoronary Doppler measurements confirmed the extremely slow blood flow velocity, the coronary flow reserve and the calculated coronary blood flow proved to be within normal range. The present findings suggest that, in contrast with a previous hypothesis, the phenomenon of slow dye progression may not always be due to a microvascular cause. Epicardial artery disease, as suggested by the marked coronary artery ectasia, may be linked to the slow dye progression and predispose to coronary artery thrombosis.

Blood Flow Velocity↗
PubMed1991

Long-term prognosis of male patients with an isolated chronic occlusion of the left anterior descending coronary artery.

The purpose of this study was to determine the long-term prognosis of patients with an isolated total occlusion of the left anterior descending artery (LAD). A total of 173 male patients with a chronic LAD occlusion and less than 50% narrowing of the other coronary arteries (group I) was compared with a group of 177 male patients with only insignificant coronary artery disease and a normal left ventricular function (group II). Baseline characteristics of both groups were comparable except for the inclusion of 54 patients (31.2%) with moderately or markedly reduced left ventricular systolic function in group I. During an 8-year follow-up period there was a greater number of patients with cardiac events in group I when compared with group II: cardiac death 11.2% versus 0.6% (p less than 0.0001), myocardial infarction 12.7% versus 3.4% (p = 0.001), myocardial revascularization procedures 11.6% versus 3.4% (p = 0.04). Stepwise discriminant analysis showed that a reduced ejection fraction and a family history of coronary artery disease were the best predictors for these adverse cardiac events.

Belgium↗
PubMed1991

The value of the intracoronary electrogram for the early detection of myocardial ischaemia during coronary angioplasty.

The clinical value of intracoronary electrography for the detection of myocardia ischaemia was assessed during coronary angioplasty and compared to a standard technique of surface ECG monitoring. In 73 patients undergoing single lesion angioplasty, an intracoronary electrogram and four representative surface ECG leads were obtained. During angioplasty of the left anterior descending artery leads, I, V3, V5, V6 were recorded. For the circumflex artery leads I, aVL, aVF, V6, and for the right coronary artery leads II, III, aVF, V6 were monitored. Eight patients were excluded due to transient intraventricular conduction disturbances during balloon inflation; 65 patients remained for further analysis. Out of a total of 154 balloon inflations (35 in the circumflex, 71 in the left anterior descending and 48 in the right coronary artery), the percentage that produced a greater than or equal to 1 mm ST segment elevation, the time to the appearance of a greater than or equal to 1 mm ST segment elevation and the maximal ST segment elevation were recorded. During inflations in the circumflex artery, the respective values of these three parameters were 20%, 22.6 +/- 11.5 s and 0.37 +/- 0.80 mm in V6, the most sensitive surface lead, versus 70% (P less than 0.001), 14.4 +/- 9.6 s (P less than 0.01) and 5.82 +/- 6.35 mm (P less than 0.0001) on the intracoronary electrogram.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1991

Torsades de pointes after intracoronary papaverine.

Coronary blood flow velocity and coronary flow reserve can be assessed in humans using a coronary Doppler catheter and the vasodilator papaverine. Although it is a safe, elegant and reproducible technique, serious complications can occur. Coronary flow reserve assessment in a 49-year-old man with a critical stenosis in the proximal part of the circumflex artery was complicated by a papaverine-induced ventricular arrhythmia. Several features of the present case report support papaverine-induced disturbances of the repolarization phase as the pathophysiological mechanism: a 'torsade de pointes' pattern of the tachycardia, the lengthening of the QT-interval, the appearance of a new U-wave and the presence of additional risk factors (hypokalaemia and alcalosis). Patients presenting additional risk factors for this complication should be excluded from coronary flow reserve assessment.

Angioplasty, Balloon, Coronary↗
PubMed1991

Silent ischaemia: an update on current concepts.

Angina pectoris is the cardinal symptom of coronary heart disease and is a symptom with which physicians are very familiar. The clinical diagnosis of ischaemic heart disease is often based largely on a history of typical chest or arm pain, and the major therapeutic endeavour in such patients is directed towards abolition or amelioration of angina. Indeed physicians have, at least up until recently, been confident in assuming that angina is a reliable marker of ongoing ischaemia and that success of medical or surgical treatment of coronary heart disease can be accurately gauged according to improvement or disappearance of anginal symptoms (Cohn & Braunwald, 1988). However, the results of a number of important clinical studies, reported over that last 10 to 15 years, appear to challenge these traditional medical assumptions. In many patients with coronary heart disease, acute episodes of myocardial ischaemia are frequently unaccompanied by angina, often referred to as "silent myocardial ischaemia" (Epstein et al., 1988; Fox, 1988; Cohn, 1985; Maseri, 1985). It has to be pointed out that not all painless ischaemic episodes are truly silent. Instead of experiencing pain during some episodes of acute myocardial ischaemia, patients may, on occasion, instead report symptoms such as dyspnoea or palpitations (these symptoms being known as "anginal equivalents") (Cohn & Braunwald, 1988). Nevertheless, the great majority of painless ischaemic episodes are, truly silent and not accompanied by "anginal equivalents", which has led to the trend in the recent literature to regard the terms "silent" and "painless" myocardial ischaemia as synonymous.

Coronary Disease↗
PubMed1989

Effect of intravenous diltiazem on myocardial ischemia occurring during percutaneous transluminal coronary angioplasty.

To investigate the antiischemic efficacy of intravenously administered diltiazem, 42 patients were randomly allocated to receive placebo or active treatment before 1-vessel percutaneous transluminal coronary angioplasty (PTCA). The development of myocardial ischemia was studied using subjective (pain) and objective (electrocardiography) parameters. Pretreatment with intravenous diltiazem resulted in a significantly delayed onset of ischemic pain and ST-segment elevation; these variables also returned to baseline earlier after balloon deflation. Thus, intravenous diltiazem prevents or delays the onset of myocardial ischemia during repetitive transient coronary occlusions; improvement of the myocardial blood flow distal to the coronary occlusion or impedance of calcium entry into the ischemic cell are considered as possible mechanisms. Because PTCA is increasingly used in patients with poor left ventricular function and more extensive disease, and because recent evidence suggests that better PTCA results could be obtained by the use of longer inflation times, the addition of diltiazem to the classic armamentarium could be beneficial.

Angina Pectoris↗
PubMed1989

Phospholipid-protein interactions of the plasma-membrane Ca2+-transporting ATPase. Evidence for a tissue-dependent functional difference.

The aim of the present work was to investigate the stimulation of the plasma-membrane Ca2+-transporting ATPase by negatively charged phospholipids. The Ca2+-transporting ATPase was purified from pig stomach smooth muscle and from pig erythrocytes, and was reactivated with phosphatidylcholine (PC) in the presence and absence of negatively charged phospholipids. The substitution of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidic acid (PA) or phosphatidylserine (PS) for PC induced profound changes in the Vmax, the K0.5 and the Hill coefficient of the Ca2+-activation curves for both ATPases. Low concentrations of each of the negatively charged phospholipids increased the Vmax., but high ratios of PIP, PIP2 or PA to PC decreased this parameter. PI, PA and PS increased the Vmax. of the erythrocyte enzyme to a larger extent than that of the smooth-muscle enzyme. This difference was less pronounced for PIP and absent for PIP2. PI (greater than 20% PC substituted), PIP, PIP2, PA and PS all increased the affinity of the two Ca2+-transporting ATPases for Ca2+ in the following order of potency: PIP2 greater than PIP greater than PI approximately PS approximately PA. PI, PA and PS increased the Ca2+ affinity of the smooth-muscle enzyme more than that of the erythrocyte enzyme; this difference was less pronounced for PIP and absent for PIP2. Even in the presence of calmodulin, all of the negatively charged phospholipids were still able to increase the Vmax. of the erythrocyte enzyme, whereas only PIP and PIP2 increased the affinity for Ca2+. The effect of PI at low concentrations (less than 20%) on the erythrocyte enzyme was peculiar in that it caused a decrease in the Ca2+ affinity instead of an increase. This effect was not observed for the smooth-muscle enzyme. All of the negatively charged phospholipids slightly increased the Hill coefficient for Ca2+ of both ATPases, and this effect was additive to that of calmodulin. The stimulation of the erythrocyte enzyme exhibited positive co-operativity towards PI and PIP, whereas that of the smooth-muscle enzyme did not. It is concluded (1) that there is a correlation between the number of negative charges on the phospholipids (PIP2 greater than PIP greater than PA approximately PI approximately PS) and the magnitude of their effect on the Vmax. and the K0.5 for Ca2+, and (2) that the action of the lipids on the smooth-muscle enzyme differs from that on the erythrocyte enzyme, indicating that these two Ca2+-transporting ATPases are not the same.

Animals↗
PubMed1989

Fatal aortic rupture: an unusual complication of percutaneous balloon valvuloplasty for acquired valvular aortic stenosis.

A case report complicated by a perforation of the ascending aorta during percutaneous balloon valvuloplasty for acquired aortic stenosis in a bicuspid aortic valve is presented. The clinical and pathological findings are discussed. It is suggested that in patients with hard calcified valve cusps and calcifications of the aortic annulus balloon sizes exceeding the aortic diameter should be avoided.

Aged↗
PubMed1988

Cyclic GMP-dependent protein kinase stimulates the plasmalemmal Ca2+ pump of smooth muscle via phosphorylation of phosphatidylinositol.

The effect of phosphorylation by cyclic GMP-dependent protein kinase (G-kinase) on the activity of the plasmalemmal Ca2+-transport ATPase was studied on isolated plasma membranes and on the ATPase purified from pig erythrocytes and from the smooth muscle of pig stomach and pig aorta. Incubation with G-kinase resulted, in both smooth-muscle preparations, but not in the erythrocyte ATPase, in a higher Ca2+ affinity and in an increase in the maximal rate of Ca2+ uptake. Cyclic AMP-dependent protein kinase (A-kinase) did not exert such an effect. The stimulation of the (Ca2+ + Mg2+)-dependent ATPase activity of the purified Ca2+ pump reconstituted in liposomes depended on the phospholipid used for reconstitution. The stimulation of the (Ca2+ + Mg2+)-ATPase activity by G-kinase was only observed in the presence of phosphatidylinositol (PI). G-kinase, but not A-kinase, stimulated the phosphorylation of PI to phosphatidylinositol phosphate (PIP) in a preparation of (Ca2+ + Mg2+)-ATPase obtained by calmodulin affinity chromatography from smooth muscle, but not in a similar preparation from erythrocytes. Adenosine inhibited both the phosphorylation of PI and the stimulation of the (Ca2+ + Mg2+)-ATPase by G-kinase. In the absence of G-kinase the (Ca2+ + Mg2+)-ATPase was stimulated by the addition of PIP, but not by PI. In contrast with previous results of Furukawa & Nakamura [(1987) J. Biochem (Tokyo) 101, 287-290], no convincing evidence for a phosphorylation of the (Ca2+ + Mg2+)-ATPase was found. Evidence is presented showing that the apparent phosphorylation occurs in a contaminant protein, possibly myosin light-chain kinase. It is proposed that G-kinase stimulates the plasmalemmal Ca2+ pump of smooth-muscle cells indirectly via the phosphorylation of an associated PI kinase.

Animals↗
PubMed1988

AlF4- reversibly inhibits 'P'-type cation-transport ATPases, possibly by interacting with the phosphate-binding site of the ATPase.

The only known cellular action of AlF4- is to stimulate the G-proteins. The aim of the present work is to demonstrate that AlF4- also inhibits 'P'-type cation-transport ATPases. NaF plus AlCl3 completely and reversibly inhibits the activity of the purified (Na+ + K+)-ATPase (Na+- and K+-activated ATPase) and of the purified plasmalemmal (Ca2+ + Mg2+)-ATPase (Ca2+-stimulated and Mg2+-dependent ATPase). It partially inhibits the activity of the sarcoplasmic-reticulum (Ca2+ + Mg2+)-ATPase, whereas it does not affect the mitochondrial H+-transporting ATPase. The inhibitory substances are neither F- nor Al3+ but rather fluoroaluminate complexes. Because AlF4- still inhibits the ATPase in the presence of guanosine 5'-[beta-thio]diphosphate, and because guanosine 5'-[beta gamma-imido]triphosphate does not inhibit the ATPase, it is unlikely that the inhibition could be due to the activation of an unknown G-protein. The time course of inhibition and the concentrations of NaF and AlCl3 required for this inhibition differ for the different ATPases. AlF4- inhibits the (Na+ + K+)-ATPase and the plasmalemmal (Ca2+ + Mg2+)-ATPase noncompetitively with respect to ATP and to their respective cationic substrates, Na+ and Ca2+. AlF4- probably binds to the phosphate-binding site of the ATPase, as the Ki for inhibition of the (Na+ + K+)-ATPase and of the plasmalemmal (Ca2+ + Mg2+)-ATPase is shifted in the presence of respectively 5 and 50 mM-Pi to higher concentrations of NaF. Moreover, AlF4- inhibits the K+-activated p-nitrophenylphosphatase of the (Na+ + K+)-ATPase competitively with respect to p-nitrophenyl phosphate. This AlF4- -induced inhibition of 'P'-type cation-transport ATPases warns us against explaining all the effects of AlF4- on intact cells by an activation of G-proteins.

Adenosine Triphosphatases↗
PubMed1988

An unusual case of guide wire fracture during percutaneous transluminal coronary angioplasty.

We report a case of guide wire fracture during percutaneous transluminal coronary angioplasty, using one of the newer catheter systems. The broken free end of the guide wire remained within the coronary tree, and surgical removal was necessary. Entrapment and overcoiling of the guide wire can cause fracture; in our case excessive bending in a tortuous coronary tree resulted in this unusual complication. An excessive tensile load to the guide wire may result from anatomical peculiarities and can cause wire fracture.

Angioplasty, Balloon↗
PubMed1988

Ca2+-transport ATPases of vascular smooth muscle.

To characterize the Ca2+-transport properties of the plasma membrane and of the endoplasmic reticulum of bovine pulmonary artery, membrane vesicles are subfractionated by a procedure of density-gradient centrifugation that takes advantage of the selective effect of digitonin on the density of plasma-membrane vesicles. The obtained endoplasmic-reticulum fraction contains hardly any plasma-membrane vesicles, whereas the plasma-membrane fraction is still contaminated by a substantial amount of endoplasmic-reticulum vesicles. An adenosine 5'-triphosphate (ATP) energized Ca2+-transport system and a Ca2+-stimulated ATPase activity are present in both subcellular fractions. The Ca2+ transport by the plasma membrane is catalyzed by a (Ca2+,Mg2+)-ATPase of Mr 130,000. It binds calmodulin and it has a low steady-state phosphoprotein intermediate level. The endoplasmic-reticulum vesicles contain a Ca2+-transport ATPase of Mr 100,000 that is characterized by a high steady-state phosphointermediate level. It is antigenically related to the Ca2+-pump protein of cardiac sarcoplasmic reticulum. Phospholamban, the regulatory protein of the Ca2+-transport enzyme of cardiac sarcoplasmic reticulum, is also present in the endoplasmic reticulum of the pulmonary artery. A comparison of these fractions with the previously characterized fractions from porcine gastric smooth muscle reveals important differences in the basal Mg2-ATPase activity, in the ratio of the (Ca2+,Mg2+)-ATPase of the plasmalemma to that of the endoplasmic reticulum, and in the ratio of the (Na+,K+)-ATPase activity to the plasmalemmal (Ca2+,Mg2+)-ATPase activity. These differences can be ascribed in part to the species and in part to the tissue. These data suggest that in the bovine pulmonary artery the Ca2+ extrusion via the ATP-dependent Ca2+ pump may have a less predominant role, and that the Ca2+ uptake by the endoplasmic reticulum, and possibly also the Ca2+ extrusion via the Na+-Ca2+ exchanger could be more important in this tissue than in the porcine stomach.

Adenosine Triphosphatases↗
PubMed1988

The (Ca2+-Mg2+)-ATPases of the plasma membrane and of the endoplasmic reticulum in smooth muscle cells and their regulation.

Smooth muscle cells contain two distinct Ca2+-transport ATpases with a different subcellular localization. The plasmalemmal Ca2+ pump has a relative molecular weight (Mr) of 140k and its phospho-intermediate level is increased by La3+. Its resemblance to the erythrocyte Ca2+ pump is further confirmed by its calmodulin-binding capacity and its antigenic properties. A 100k Ca2+-transport ATPase is localized in the endoplasmic reticulum. Its phospho-intermediate level is decreased by La3+, and it is antigenically related to the cardiac sarcoplasmic reticulum Ca2+-transport ATPase. These two different Ca2+-transport ATPases are present in both visceral and vascular smooth muscle, but tissue- and species-dependent differences in their relative amount have been observed. The endoplasmic-reticulum Ca2+-transport ATPase is regulated via phospholamban. Phosphorylation of this regulatory protein by cAMP-dependent as well as by cGMP-dependent protein kinase stimulates the endoplasmic-reticulum Ca2+ pump. The activity of the plasmalemmal Ca2+-transport ATPase can be modulated by calmodulin, negatively charged phospholipids, and by receptor-binding agonists. cGMP-dependent protein kinase also exerts a stimulatory effect on the plasmalemmal Ca2+ pump, but this effect is not mediated via a direct phosphorylation of the Ca2+ pump.

Animals↗