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S H Monnink

Publications and source records attributed to S H Monnink.

10 recordsLinked to original sources
PubMed2000

Comparison of zofenopril and lisinopril to study the role of the sulfhydryl-group in improvement of endothelial dysfunction with ACE-inhibitors in experimental heart failure.

We evaluated the role of SH-groups in improvement of endothelial dysfunction with ACE-inhibitors in experimental heart failure. To this end, we compared the vasoprotective effect of chronic treatment with zofenopril (plus SH-group) versus lisinopril (no SH-group), or N-acetylcysteine (only SH-group) in myocardial infarcted (MI) heart failure rats. After 11 weeks of treatment, aortas were obtained and studied as ring preparations for endothelium-dependent and -independent dilatation in continuous presence of indomethacin to avoid interference of vasoactive prostanoids, and the selective presence of the NOS-inhibitor L-NMMA to determine NO-contribution. Total dilatation after receptor-dependent stimulation with acetylcholine (ACh) was attenuated (-49%, P<0.05) in untreated MI (n=11), compared to control rats with no-MI (n=8). This was in part due to impaired NO-contribution in MI (-50%, P<0.05 versus no-MI). At the same time the capacity for generation of biologically active NO after receptor-independent stimulation with A23187 remained intact. Chronic treatment with n-acetylcysteine (n=8) selectively restored NO-contribution in total dilatation to ACh. In contrast, both ACE-inhibitors fully normalized total dilatation to ACh, including the part mediated by NO (no significant differences between zofenopril (n=10) and lisinopril (n=8)). Zofenopril, but not lisinopril, additionally potentiated the effect of endogenous NO after A23187-induced release from the endothelium (+100%) as well as that of exogenous NO provided by nitroglycerin (+22%) and sodium nitrite (+36%) (for all P<0.05 versus no-MI). We conclude that ACE-inhibition with a SH-group has a potential advantage in improvement of endothelial dysfunction through increased activity of NO after release from the endothelium into the vessel wall. Furthermore, this is the first study demonstrating the selective normalizing effect of N-actylcysteine on NO-contribution to ACh-induced dilatation in experimental heart failure.

Acetylcholine↗
PubMed2000

Functional integrity and aging of the left internal thoracic artery after coronary artery bypass surgery.

OBJECTIVE: To study the endothelial function in the left internal thoracic artery after coronary artery bypass surgery and to identify predictors of early dysfunction, we performed a provocative test with acetylcholine in 23 male patients who underwent routine postoperative coronary angiography. METHODS: The change in mean diameter of the proximal thoracic artery was assessed by quantitative angiography after selective injections of acetylcholine and nitroglycerin. RESULTS: The thoracic artery showed a 6.8% (P <. 001) and 9.0% (P <.001) increase in mean diameter after acetylcholine and nitroglycerin administration, respectively. Vasodilative responses to acetylcholine and nitroglycerin administration were strongly correlated (R: 0.88; P <.001). Among the common risk factors, only age was associated with an impairment in the vasodilative response of the arterial graft (P =.001), and acetylcholine-induced vasodilation was inversely correlated to the age of the patient (R: 0.69; P <.001). CONCLUSIONS: Endothelium-dependent vasodilative response to acetylcholine administration seems well preserved in the left internal thoracic artery after surgery. Common risk factors, except for age, do not affect the functional integrity of the arterial graft. The vasodilative properties of the graft depend on the age of the patient and do not deteriorate over time after operation.

Acetylcholine↗
PubMed1999

Humoral immune response to human cytomegalovirus in patients undergoing percutaneous transluminal coronary angioplasty.

Possible causal relations between prior human cytomegalovirus (HCMV) infection and atherosclerosis and between HCMV reactivation and restenosis after coronary angioplasty have been suggested. We investigated patterns of antibodies directed to HCMV in 112 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) and in a group of sex- and age-matched controls (blood donors without evidence of atherosclerosis). Levels of antibodies to HCMV were measured by enzyme-linked immunosorbent assay (ELISA) of serum samples drawn before and 5 weeks after PTCA. To further differentiate the humoral immune response, we specifically tested antibody reactivity towards four single HCMV proteins (IE2, p52, pp150, and pp65) by recombinant ELISAs. We found that 73% of PTCA patients and 69% of sex- and age-matched controls were seropositive for HCMV (odds ratio, 1.2 [not significant]). The corresponding odds ratios for matched pairs ranged in the recombinant ELISAs from 1.2 to 1.4. Patients had more often high titers of anti-HCMV antibodies (11 versus 4%; odds ratio = 3.3 [0.9 to 15.2]; P = 0.052) and high titers of anti-pp150 antibodies (13 versus 4%; odds ratio = 6.0 [1.3 to 38.8]; P = 0.008). Anti-HCMV immunoglobulin M antibodies were not detected in any patient. There was no evidence of acute HCMV reactivation after PTCA, since the titers of antibodies to the investigated recombinant proteins did not increase at 5 weeks after PTCA. Our results show a limited association between prior HCMV infection and coronary artery disease. We infer that positive anti-HCMV titers are not a major risk factor at the time of disease manifestation. However, this study cannot rule out a possible role of HCMV at earlier stages of the atherosclerotic process. Recombinant ELISAs provide a valuable tool for investigating the antiviral immune response.

Adult↗
PubMed1999

Silicon-carbide coated coronary stents have low platelet and leukocyte adhesion during platelet activation.

BACKGROUND: Stent thrombosis and restenosis are of great clinical significance. We constructed a closed loop in vitro heparinized whole human blood circulation model for testing hemocompatibility of coronary stents. This model allows evaluation of human blood activation by blood-stent interaction in a well-controlled setting. Until now these interactions were studied in the highly coagulable pig coronary artery model. METHODS: We evaluated activation of the coagulation system and blood components by uncoated, heparin-coated, and silicon-carbide coated tantalum stents. The effects, measured by biochemical assays, were compared with stainless-steel stents. Also the inhibitory effect on platelet activation by indomethacin equal to the oral effect of 325 mg acetylsalicylic acid daily, was measured and visualized by scanning electron microscopy. RESULTS: Both activation of the coagulation system and platelets were counteracted by indomethacin, suggesting an important role for platelets in activation of the coagulation system in this model. Despite platelet activation by all stents, the SiC-coated tantalum stent demonstrates a significantly lower GpIIIa receptor-mediated platelet adhesion at the stent surface (21.7 x 10(3) counts per second/mg stent weight) compared to all other stents (stainless-steel 54.0, heparin-coated 95.7 and uncoated 76.2 x 10(3) cps/mg). Also activated leukocytes demonstrated a significantly lower CD11b receptor-mediated adhesion at the SiC-coated stent (37.0 x 10(3) cps/mg) than at the stainless-steel stent (114.5 x 10(3) cps/mg). CONCLUSIONS: Data from this in vitro circulation study show a significantly lower platelet and leukocyte adhesion at the surface of the SiC-coated tantalum stent than at the surface of stainless-steel stents or uncoated and heparin-coated tantalum stents.

Blood Platelets↗
PubMed1998

Prior cytomegalovirus infection does not predict clinical outcome after percutaneous transluminal coronary angioplasty.

BACKGROUND: A direct association between human cytomegalovirus (HCMV) infection and the development of restenosis after coronary angioplasty has been suggested. The aim of this prospective study was to evaluate the value of HCMV serology in predicting the clinical outcome after percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: 112 patients undergoing elective PTCA were included in the study. HCMV antibody levels were measured by ELISA. Cardiac events within a follow-up period of 6 months after PTCA were defined as (1) progression or recurrence of anginal complaints and/or a positive exercise test; (2) restenosis that required repeat revascularization. 73% of PTCA patients were seropositive for HCMV. Successful PTCA was achieved in a total of 94 patients, who were followed for 6 months. In 31/94 patients (33%) cardiac events occurred and in 15/94 (16%), this could be related to restenosis. We found no statistically significant difference between seropositive and negative patients with respect to anginal complaints or the need for revascularization. There was no evidence of acute reactivation, since titers of anti-HCMV antibodies did not increase after PTCA. CONCLUSION: This study shows that the clinical outcome after PTCA is not related to the HCMV serostatus of the patient. Therefore, our data do not support the hypothesis that serological markers of HCMV infection are of clinical importance for the assessment of a patient's individual risk after PTCA. This does not preclude a role for local reactivation of HCMV at the site of angioplasty.

Acute Disease↗
PubMed1997

Minimally invasive coronary artery bypass grafting versus coronary angioplasty for isolated type C stenosis of the left anterior descending artery.

BACKGROUND: Isolated stenosis of the left anterior descending coronary artery can be treated with medication, percutaneous transluminal coronary angioplasty, or coronary artery bypass grafting. Recently a new treatment has been developed, which is called minimally invasive direct coronary artery bypass grafting. This new treatment is a modification of the conventional bypass operation and is performed through a small anterolateral thoracotomy without cardiopulmonary bypass. METHODS: To compare minimally invasive bypass with angioplasty, we evaluated in-hospital results and 1-year follow-up in 181 consecutive patients with isolated type C stenosis of the left anterior descending coronary artery between January 1995 and July 1996. Of these patients, 71 underwent minimally invasive bypass and 110 angioplasty. Preoperative characteristics were not significantly different between the two groups. RESULTS: In-hospital death, periprocedural myocardial infarction, emergency reoperation by means of conventional coronary bypass grafting, use of an intraaortic balloon pump, and cerebrovascular accidents were not significantly different between the two groups. At 1-year follow-up, survival was not significantly different in the two groups (minimally invasive bypass 95.7% +/- 0.2% vs angioplasty 95.3% +/- 0.2%; p = 0.89), whereas freedom from repeated revascularization was significantly more common in the group undergoing minimally invasive bypass (bypass 96.9% +/- 0.2% vs angioplasty 67.6% +/- 0.5%; p < 0.001). This study shows that the need for repeated revascularization, and therefore the use of health care resources, is significantly less with minimally invasive bypass than with angioplasty in patients with isolated type C stenosis of the left anterior descending coronary artery.

Angioplasty, Balloon, Coronary↗
PubMed1995

Retransfusion of suctioned blood during cardiopulmonary bypass impairs hemostasis.

In a previous study we observed extensive clotting and fibrinolysis in blood from the thoracic cavities during cardiopulmonary bypass. We hypothesized that retransfusion of this suctioned blood could impair hemostasis. In this prospective clinical study we investigated the effect of suctioned blood retransfusion on systemic blood activation and on postoperative hemostasis. During coronary artery bypass grafting in 40 patients, suctioned blood was collected separately. It then was retransfused to the patient at the end of the operation (n = 19), or it was retained (n = 21). During the study, 12 consecutive patients, randomized in two groups of 6, were analyzed for biochemical parameters indicating blood activation and clotting. The immediate and significant increase in circulating concentrations of thrombin-antithrombin III complex, tissue-type plasminogen activator, fibrin degradation products, and free plasma hemoglobin demonstrated the effect of suctioned blood retransfusion. Moreover, the increased concentrations of thrombin-antithrombin III complex and fibrin degradation products indicated renewed systemic clotting and fibrinolysis as a direct result of the retransfusion of suctioned blood. Concentrations of all indicators mentioned remained significantly lower in the retainment group. The clinical data showed that retainment of suctioned blood resulted in significantly decreased postoperative blood loss (822 mL in the retransfusion group versus 611 mL in the retainment group; p < 0.05) and similar or even reduced consumption of blood products (513 versus 414 mL red blood cell concentrate and 384 versus 150 mL single-donor plasma; both not significant). We conclude that retransfusion of highly activated suctioned blood during cardiopulmonary bypass exacerbates wound bleeding.

Blood Transfusion, Autologous↗
PubMed1995

Platelet function analysis after in vitro treatment with hemostasis-affecting components.

An overall platelet function test in whole blood, which simulates conditions under arterial pressure, is useful in measuring the effect of polymer materials on blood hemostatic function. We performed biocompatibility tests with materials or plasma substitutes by interaction of blood from healthy volunteers and then subjected these blood samples to platelet function analysis (Thrombostat). We tested also the capacity of locally applied hemostatic agents for bleeding control by direct application of these agents onto the Thrombostat measuring cell. The biocompatibility tests with materials exposed to blood appeared very discriminating between compatible and noncompatible materials. The hemostatic capacity of blood exposed to noncompatible materials (assessed by binding of active thrombin) reduced markedly after one hour incubation of the material. The plasma substitutes did not affect hemostasis significantly. However, a blood dilution of 40%, as in cardiopulmonary bypass, increased the time required for closure of the measuring cell by a platelet plug exponentially. Local hemostatic agents could be selected according to their capacity to enhance platelet plug formation. In addition, ADP mixed with the hemostatic agent was most effective in improving capacity. We conclude that platelet function analysis contributes importantly to screening of materials and plasma substitutes with regard to their interaction with primary hemostasis.

Biocompatible Materials↗
PubMed1992

Captopril modifies the response of infarcted rat hearts to isoprenaline stimulation.

In this study the effect of the angiotensin converting enzyme (ACE) inhibitor captopril on beta-receptor responsiveness was investigated in failing rat hearts after experimental myocardial infarction. Infarcted rats were treated for 8 weeks with either captopril added to the drinking water (100 mg/kg/day; n = 5) or drinking water alone (n = 7). Treatment was started 2-3 days before myocardial infarction. A third group of untreated rats without myocardial infarction served as control (n = 6). At the end of the treatment period the hearts were perfused as described by Langendorff, and a cumulative dose-response curve of isoprenaline was obtained in each heart. In comparison with noninfarcted hearts, the response of heart rate and peak pressure rate (dP/dt) to isoprenaline stimulation was significantly depressed in hearts of infarcted rats. Chronic treatment with captopril significantly attenuated the reduced responsiveness to isoprenaline stimulation. This improved responsiveness in captopril-treated rat hearts might be due to prevention of "down-regulation" of myocardial beta-adrenoceptors. Other factors should also be considered, such as prevention of structural alterations in the noninfarcted myocardium, e.g., myocardial hypertrophy and fibrosis. Differences in infarct size did not play an important role, since infarct size was comparable in both groups of infarcted rats. This partial preservation of beta-adrenergic responsiveness was accompanied by a significant reduction in right ventricular weight and lung weight, suggesting that captopril also improved the signs of heart failure. Therefore, the results of this study indicate that early ACE inhibition in myocardial infarction may be useful in preventing deterioration of cardiac function.

Administration, Oral↗