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Biomedical subjects

M Gottsauner-Wolf

Publications and source records attributed to M Gottsauner-Wolf.

At least 19 recordsLinked to original sources
PubMed2005

Predictive value of plasma plasminogen activator inhibitor-1 for coronary restenosis: dependence on stent implantation and antithrombotic medication.

BACKGROUND: The plasmin activation system is involved in the development of restenosis after percutaneous coronary interventions (PCI). Conflicting data exist concerning the role of plasminogen activator inhibitor-1 (PAI-1) and its predictive value for restenosis. OBJECTIVES: To evaluate the fibrinolytic response to injury after PCI with or without stent implantation on different antithrombotic medications and its relation to late restenosis. PATIENTS AND METHODS: Eighty consecutive patients with successful PCI without (balloon only; n = 37) or with stent implantation (stent; n = 43) on different antithrombotic regimes (balloon only, aspirin; stent, aspirin/coumadin/dipyridamole vs. aspirin/ticlopidine). Blood samples were taken at baseline and up to 7 days after PCI and PAI-1 active antigen and tissue plasminogen activator (t-PA) antigen were determined. Restenosis was angiographically determined after 6 months. RESULTS: PCI increased both t-PA and PAI-1 levels (P < 0.001), with a significant prolonged and pronounced increase in stent vs. balloon-only patients (P < 0.05). Restenosis (stent 26%; balloon 38%) was significantly correlated to an attenuated PAI-1 increase after 24 h in the ticlopidine group (P = 0.007; restenosis, relative Delta PAI-1 + 50 +/- 28%; non-restenosis, + 139 +/- 50%), but not in the coumadin group. In the balloon-only group late restenosis (ISR) was associated with a trend for an augmented PAI-1 increase after 24 h. CONCLUSIONS: Coronary stent implantation significantly increases t-PA and PAI-1 plasma levels up to 1 week compared with balloon angioplasty alone. ISR in ticlopidine-treated patients was associated with an attenuated early PAI-1 active antigen increase. A less than 50% increase 24 h after stent implantation under ticlopidine treatment may identify patients at risk for the development of ISR.

Aged↗
PubMed2003

Percutaneous interventions in radiation-associated coronary in-stent restenosis.

This study was performed to evaluate the outcome of percutaneous revascularization in "edge restenoses" developing after radioactive stent implantation in de novo and in-stent lesions. Twenty-one consecutive patients undergoing target lesion revascularization (TLR) at any follow-up after phosphorus-32 radioactive stent implantation were included in this study. We assessed the incidence of death, myocardial infarction, repeated TLR and recurrent angina over the following 18 months. After 6 months, TLR rate was 28.6%, and no stent thromboses, deaths or Q-wave myocardial infarctions occurred. Among the patients with TLR there were significantly more subjects who had received a radioactive stent in a previous in-stent restenosis (66.7% vs. 0% in patients without second restenosis; P <0.001), or who had received two radioactive stents (83.3% vs. 33.3%; P = 0.038). After 18 months, TLR rate was 33.3%, and two patients (9.5%) had died. Restenosis after intravascular radiotherapy can be safely treated by percutaneous interventional techniques, yielding an acceptable clinical result within 18 months.

Adult↗
PubMed2001

[Chlamydia antibody titers in patients with coronary disease: relations to age and clinical stage].

BACKGROUND AND AIM: Atherosclerosis and its clinical sequelae are responsible for the highest death rate in industrialized countries. Seroepidemiological, pathological and immunohistochemical studies have suggested a relation between Chlamydia pneumoniae infection and the development of coronary sclerosis. Aim of this study was to investigate the frequency distribution of Chlamydia pneumoniae antibody titers in patients with different clinical stages of coronary artery disease (CAD) and patients without CAD as well as a possible age dependence of antibody titers within the study groups. For this purpose, 522 consecutive patients of a cardiology ward were investigated, over a period of 10 months, for the presence of Chlamydia pneumoniae antibodies (IgG, IgA, IgM) using specific ELISA's. In general, there was no difference in the frequency of positive Chlamydia antibody titers between CAD patients and the control group. Only in the subgroup of unstable CAD-patients < 50 years a tendency of increased antibody titers was present. Patients with stable angina, unstable angina, or acute myocardial infarction exhibited no significant differences in the rate of infection between the different age groups (p < 0.117). In contrast, there was a significant increase in positive Chlamydia pneumoniae antibodies with increasing age in the control group (p = 0.002). The relatively high incidence of positive Chlamydia pneumoniae antibody titers in young CAD patients, which is associated with a loss of age-dependent increase of the antibody titers in the CAD group, might indicate a specific role of Chlamydia pneumoniae infections for the manifestation of premature CAD (before the age of 50). Due to the increased rate of Chlamydia pneumoniae infections with increasing age, the determination of Chlamydia pneumoniae antibody titers does not allow reliable conclusions on the infectious pathogenesis of CAD. Furthermore, our unability to demonstrate differences in antibody titers between CAD patients with stable angina, unstable angina, and acute myocardial infarction suggests that acute Chlamydia pneumoniae infections are not responsible for the development of acute coronary syndromes.

Age Factors↗
PubMed2001

PAI-I 4G/5G polymorphism and sudden cardiac death in patients with coronary artery disease.

UNLABELLED: The 4G/5G polymorphism of the plasminogen activator inhibitor type I (PAI-I) gene is involved in coronary artery disease (CAD), with the highest risk in 4G/4G homozygotes. The role of PAI-I polymorphism in patients suffering from CAD and history of sudden cardiac death (SCD) has not been addressed yet. We studied the frequency distribution of the PAI-I gene to test the hypothesis that the 4G/4G genotype favors myocardial ischemia and, even in the absence of acute infarction, promotes SCD in patients with CAD. METHODS: The PAI-I 4G/5G genotypes and PAI-I antigen plasma levels were determined in 97 patients with CAD and a history of SCD treated with an implantable cardioverter defibrillator (ICD) (defibrillator group) comparing to 113 patients with CAD but no history of SCD (control group). RESULTS: The defibrillator group consisted of significantly more 4G/4G homozygotes and higher PAI-I levels than the control group (44% vs. 24%, 173+/-41 vs. 144+/-49 ng/ml; P<.01). The carriers of 4G allele had a significantly higher risk for SCD (odds ratio (OR) 1.9) with the highest risk in the 4G/4G genotype (OR 3.6, P<.01). CONCLUSION: These results suggest that the PAI-I 4G/4G genotype is associated with SCD in patients suffering from CAD.

Aged↗
PubMed2001

An iatrogenic coronary arteriovenous fistula causing a steal phenomenon: an intracoronary Doppler study.

We present the case of a 67-year-old man in whom a guidewire broke at rotablation of the right coronary artery, creating an iatrogenic aneurysmal arteriovenous fistula to the coronary sinus. Successful Doppler wire-guided fistula occlusion by percutaneous coil embolization lead to normalization of coronary blood flow and relief of the patient's symptoms. Myocardial ischemia in this patient may have been due to a steal phenomenon caused by coronary artery fistulae, as suggested by blood flow velocity data obtained before and after fistula occlusion.

Aged↗
PubMed2001

Dose-volume histograms based on serial intravascular ultrasound: a calculation model for radioactive stents.

BACKGROUND AND PURPOSE: Radioactive stents are under investigation for reduction of coronary restenosis. However, the actual dose delivered to specific parts of the coronary artery wall based on the individual vessel anatomy has not been determined so far. Dose-volume histograms (DVHs) permit an estimation of the actual dose absorbed by the target volume. We present a method to calculate DVHs based on intravascular ultrasound (IVUS) measurements to determine the dose distribution within the vessel wall. MATERIALS AND METHODS: Ten patients were studied by intravascular ultrasound after radioactive stenting (BX Stent, P-32, 15-mm length) to obtain tomographic cross-sections of the treated segments. We developed a computer algorithm using the actual dose distribution of the stent to calculate differential and cumulative DVHs. The minimal target dose, the mean target dose, the minimal doses delivered to 10 and 90% of the adventitia (DV10, DV90), and the percentage of volume receiving a reference dose at 0.5 mm from the stent surface cumulated over 28 days were derived from the DVH plots. Results were expressed as mean+/-SD. RESULTS: The mean activity of the stents was 438+/-140 kBq at implantation. The mean reference dose was 111+/-35 Gy, whereas the calculated mean target dose within the adventitia along the stent was 68+/-20 Gy. On average, DV90 and DV10 were 33+/-9 Gy and 117+/-41 Gy, respectively. Expanding the target volume to include 2.5-mm-long segments at the proximal and distal ends of the stent, the calculated mean target dose decreased to 55+/-17 Gy, and DV 90 and DV 10 were 6.4+/-2.4 Gy and 107+/-36 Gy, respectively. CONCLUSIONS: The assessment of DVHs seems in principle to be a valuable tool for both prospective and retrospective analysis of dose-distribution of radioactive stents. It may provide the basis to adapt treatment planning in coronary brachytherapy to the common standards of radiotherapy.

Aged↗
PubMed2001

Fatal late coronary thrombosis after implantation of a radioactive stent: postmortem angiographic and histologic findings--case report.

Postmortem angiography and histologic analysis of a fatal coronary thrombosis 4 months after implantation of a radioactive stent are described. Histologic findings suggested incomplete re-endothelialization in the segment with the stent. Ionizing radiation may delay re-endothelialization after revascularization, thus maintaining the thrombogenicity of the irradiated vessel segment. Thus, prolonged antiplatelet therapy should be considered after intravascular radiation therapy.

Aged↗
PubMed2000

Design and dosimetry of a novel 90Y beta source to prevent restenosis after angioplasty.

PURPOSE: Post-dilatation irradiation of the vessel wall is currently under investigation for prevention of restenosis after balloon dilatation. For the irradiation, special sources were designed for animal experiments which would give equivalent irradiation conditions and doses to the vessel wall that would later be employed for human application. METHODS AND MATERIALS: For the planned irradiations, a specially designed yttrium-wire of 0.45-mm diameter coated with a thin shrink tube to prevent contamination was deployed. Several leakage tests applied before and after application proved that the irradiation source was leakproof. Dosimetry was performed by using 0.1-mm-thick thermoluminescent dosimeters (TLD-100) calibrated against a primary standard. A shielding transport and application container was designed to facilitate the handling of the source during use, while reducing exposure of the medical personnel. RESULTS: The designed source proves to be flexible for the insertion into proximal coronary vessels, and positioning at the site of stenosis. It provides an optimum protection of the animal and requires little radiation protection efforts on behalf of the medical staff. Dosimetric calculations and measurements showed that a centering of the source inside the vessel could be achieved with a maximum deviation of 50% between maximum and average dose levels. CONCLUSION: A yttrium-90 beta brachytherapy source was designed which provides high flexibility within proximal coronary arteries, ensures an adequate centering inside the artery, and provides irradiation conditions to the vessel wall of the experimental animal comparable to the application inside a human artery.

Angioplasty, Balloon, Coronary↗
PubMed2000

Plasma levels of C-reactive protein after coronary stent implantation.

AIMS: This study was designed to investigate the role of inflammation on the occurrence of angiographic restenosis 6 months after coronary stent implantation and the influence of different kinds of antithrombotic and antiplatelet strategies on inflammation. METHODS AND RESULTS: In an open randomized trial, 40 consecutive patients were treated with aspirin (100 mg. day(-1)) and either ticlopidine (2x250 mg. day(-1)) (n=17), or phenprocoumon (INR 2.0-3.0) and dipyridamole (3x160 mg. day(-1)) (n=23) after successful elective coronary stent implantation. Plasma levels of C-reactive protein were determined one day before stent implantation and serially thereafter twice daily up to 120 h. C-reactive protein plasma levels increased significantly (P<0.0001) after stent implantation. Phenprocoumon and dipyridamole or ticlopidine had no effect on C-reactive protein plasma levels (P=0.51) or the occurrence of angiographic restenosis (P=0.48). C-reactive protein plasma levels were significantly higher in patients with lesion type C compared to types A or B (P=0.035), respectively. C-reactive protein plasma levels were significantly higher and mean shoulder levels occurred 48 h later in patients with restenosis compared to patients without restenosis after 6 months (P=0.038). CONCLUSIONS: Elevated C-reactive protein plasma levels still persisting 96 h after stent implantation might reflect a prolonged inflammatory reaction to coronary stent implantation which might causally be involved in pathophysiological mechanisms leading to restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1999

Angiotensin-converting enzyme and angiotensin II receptor 1 polymorphism in coronary disease and malignant ventricular arrhythmias.

OBJECTIVES: It has been reported that patients carrying the angiotensin-converting enzyme (ACE) deletion DD genotype with the angiotensin II type 1 (AT1) C allele are at increased risk for myocardial infarction. The frequency distribution of the ACE and AT1 receptor gene polymorphism and their possible relation regarding malignant ventricular arrhythmias in patients with coronary artery disease (CAD) and left ventricular dysfunction was determined. METHODS: The ACE I/D and AT1 A/C polymorphisms (using polymerase chain reaction) in 100 Caucasian patients suffering from CAD with a history of malignant ventricular arrhythmias treated with an implantable cardioverter defibrillator (ICD group) was compared to 127 age-matched Caucasian patients with CAD and no history of malignant ventricular arrhythmias (control group). All patients had reduced left ventricular ejection fraction of < 40% and were comparable regarding sex distribution, body mass index, ACE-inhibitor treatment, lipid status and duration of CAD. RESULTS: The prevalence of DD/CC in the ICD group was significantly higher (19% versus 10%, p < 0.0001). The risk for malignant ventricular arrhythmias was associated with the combination of ACE D and AT1 C alleles (odds-ratio: 2.4, 95% confidence interval 1.41 to 3.94, p < 0.001). The distribution of ACE and AT1 genotypes was not different between the two group. CONCLUSIONS: Patients with coronary artery disease and left ventricular dysfunction carrying ACE D and AT1 C alleles are at increased risk for development of malignant ventricular arrhythmias. Because of available pharmacological inhibitors, these results may have clinical implications for the prevention of sudden cardiac death.

Aged↗
PubMed1999

Predictive value of PAI-1 plasma activity and thallium perfusion imaging for restenosis after percutaneous transluminal angioplasty in clinically asymptomatic patients.

BACKGROUND: The main long-term complication of percutaneous transluminal coronary angioplasty (PTCA) is restenosis that occurs in 30-50 percent of all primary successful cases. The purpose of this study was to evaluate the predictive value of changes in plasminogen activator inhibitor-1 (PAI-1) activity and of thallium dipyridamole perfusion imaging performed 3 months after successful angioplasty. All patients were asymptomatic at evaluation. The results of these two noninvasive tests were compared with the angiographic outcome after 6 months. METHOD AND PATIENTS: Twenty-five patients were included in this prospective study. All patients had single vessel disease, successful angioplasty and were free of clinical symptoms 3 months after angioplasty that would suggest late restenosis. In 12/25 patients (48%) angiographic restenosis (percent diameter stenosis >50%) was determined by follow-up angiography 6 months after angioplasty. PAI-1 plasma activity was determined by a functional titration assay and increase or decrease of PAI-1 plasma activity was evaluated between values obtained before and 3 months after angioplasty. In 7/25 (28%) patients PAI-1 plasma activity increased to more than 90% of pre-angioplasty values. This increase correlated with angiographic restenosis evaluated 6 months after angioplasty (sensitivity 42%, specificity 85%, positive predictive value 71%, and negative predictive value 61%). T1-201-perfusion imaging was performed 3 months after angioplasty. This test was indicative for subsequent restenosis in 5/25 patients (sensitivity 33%, specificity 100%, positive predictive value 62%, and negative predictive value 100%). In 10/25 (40%) patients at least one of the two non-invasive tests performed 3 months after angioplasty predicted angiographic restenosis at 6 months: the combined use of PAI-1 and T1-201-perfusion imaging resulted in increased sensitivity (67%) and high specificity (85%). CONCLUSION: The results of this study indicate that an increase of PAI-1 plasma activity may improve the predictive value for restenosis of T1-201-scintigraphy performed 3 months after angioplasty even in asymptomatic patients.

Angioplasty, Balloon, Coronary↗
PubMed1999

[Acute coronary syndromes: physiopathology and therapeutic aspects].

This article discusses recent developments in the field of acute coronary syndromes including pathophysiological mechanisms as well as therapeutic strategies. A plaque disruption is caused by different stimuli in a plaque prone to rupture, i.e. a plaque with a lipid-rich core and high local concentration of inflammatory cells (T-cells, monocytes/macrophages, mast cells). These cells are capable of producing matrix degradation products and can reduce stability of a plaque. Thrombus formation, based on platelet activation and aggregation as well as fibrin formation, is the main consequence of plaque disruption. Depending on the degree of thrombus formation occlusion is followed clinically by unstable angina (subtotal occlusion) or by acute myocardial infarction (total occlusion). Accompanying vasoconstriction may further aggravate the situation. Principles of therapy are thrombus dissolution as well as prevention of new thrombus formation: main goals of thrombolytic therapy in acute myocardial infarction are a prompt (less than 3 hours), complete, and sustained (prevention of early thrombotic reocclusion) reperfusion.

Acute Disease↗
PubMed1998

Therapeutic efficiency of lipoprotein(a) reduction by low-density lipoprotein immunoapheresis.

This study was performed to investigate the effect of low-density lipoprotein (LDL) immunoapheresis on lipoprotein(a) [Lp(a)] reduction in patients with heterozygous and homozygous familial hyperlipidemia (N=16) and insufficient response to lipid-lowering agents. By desorption of approximately 5,700+/-500 mL of plasma, a mean reduction in total cholesterol of 62% (P < .001) and in LDL-cholesterol of 70% (P < .001) was achieved. Lp(a), which was elevated at study entry in seven of these patients (82.1+/-34.3 mg/dL; range, 48 to 148 mg/dL), was reduced during the initial LDL-apheresis procedure by 74.8%+/-14.1% (P < .001). Long-term apheresis treatment performed at weekly intervals resulted in an mean reduction in Lp(a) pretreatment values to 39.1+/-28.5 mg/dL (-54%; P < .001). Desorbed Lp(a) was measured at the waste of the columns for 31 apheresis treatments. Lp(a) concentration of the column waste was higher in patients with elevated serum Lp(a) pretreatment values as compared with those with Lp(a) serum values within the normal range (elevated Lp(a), 1,420+/-380 mg; without elevated Lp(a), 235+/-190 mg; P < .001). The rate of return of Lp(a) following apheresis treatment scheduled at weekly intervals was comparable to that of LDL-cholesterol.

Adolescent↗
PubMed1998

Predictors of outcome in patients with implantable cardioverter defibrillators.

UNLABELLED: This study determined the impact of clinical characteristics on shock occurrence and survival in patients with implantable cardioverter-defibrillator (ICD). METHODS AND RESULTS: During a follow-up of 27 +/- 18 months, the actuarial incidence of appropriate shocks in 200 consecutive patients was 18, 36 and 72% at 1, 3, and 5 years, respectively. Coronary artery disease was the only significant predictor for shock occurrence (relative risk 1.32, p = 0.03). The actuarial incidence of total mortality was 10, 17 and 33% at 1, 3, and 5 years, respectively. The most powerful predictors for total mortality were: New York Heart Association functional class (NYHA) III (relative risk 4.8, p = 0.001) and a history of congestive cardiac failure (relative risk 3.6, p = 0.01). CONCLUSION: During long-term follow-up, the majority of patients receive appropriate shocks. No strong predictors for shock occurrence can be identified from the data analyzed. A history of congestive cardiac failure and the NYHA III are the most powerful predictors for total mortality. These clinical factors may provide valuable criteria to identify patients who will benefit from the implantation of ICD.

Arrhythmias, Cardiac↗
PubMed1997

Quantitative evaluation of local drug delivery using the InfusaSleeve catheter.

BACKGROUND: Restenosis is the most common long-term complication after angioplasty. Local delivery of pharmacologic agents at the site of angioplasty holds promise as a means of achieving higher concentrations of drug in the arterial wall than can be obtained by systemic infusion. In this study, a novel local drug delivery catheter system, the InfusaSleeve catheter, was evaluated in a porcine coronary balloon injury model. The purpose of the study was to evaluate the efficacy of solute transfer to the arterial wall and the influence of varying supporting angioplasty balloon pressure. METHODS AND RESULTS: Ten pigs (total of 22 arterial segments) underwent overstretch balloon injury (artery/balloon ratio 1:1.29) with a standard angioplasty balloon. In 7 animals (16 arterial segments) horseradish peroxidase (HRP; 10 mg/ml) was administered locally after injury, by tracking the local infusion catheter as a sheath over the angioplasty balloon to the intended site of arterial drug delivery. Supporting angioplasty balloons were inflated to one of the three different pressures. In 3 pigs HRP (10 mg/ml) was administered intravenously. No significant arterial injury caused by the local delivery device was evident on histological examination (disruption of the internal lamina elastica, arterial media, or thrombosis). Radial concentrations of the HRP reaction product in the first 150 microns of the arterial wall were quantified against known standards by measurement of light transmission through tissue sections. Mean HRP concentrations were not significantly different from those obtained by intravenous infusion using a supporting pressure of 1 atm or a supporting pressure of 3 atm of the underlying angioplasty balloon. However, a supporting pressure of 6 atm resulted in a 6-fold greater mean HRP concentration in the arterial wall than that which could be achieved by systemic administration of an equal volume of tracer (P < 0.001). CONCLUSION: Thus solute can be delivered throughout the coronary media by the InfusaSleeve, with the magnitude of wall uptake related to support pressure. Local delivery at 6 atm support pressure produced substantially greater uptake than did systemic delivery.

Angioplasty, Balloon, Coronary↗
PubMed1997

Influence of local delivery of the protein tyrosine kinase receptor inhibitor tyrphostin-47 on smooth-muscle cell proliferation in a rat carotid balloon-injury model.

Smooth-muscle cell proliferation in response to arterial injury represents an important etiologic factor in restenosis after angioplasty. Tyrphostin-47, a protein tyrosine kinase inhibitor, inhibits smooth-muscle cell proliferation in vitro. In this study tyrphostin-47 was incorporated into matrixes to determine whether prolonged local delivery would result in a reduction of neointimal proliferation after arterial injury in a rat carotid balloon-injury model. A polymer matrix (polylactic polyglycolic acid copolymer and pluronic gel F-127, mean matrix weight 7.83 +/- 0.39 mg) was loaded with tyrphostin-47 (25% w/w). Release studies demonstrated delivery of 11% of the incorporated drug over a 21-day release period. In cell culture, tyrphostin-47 released from the polymer matrix produced a reduction in smooth-muscle cell proliferation (p < 0.0007). Balloon denudation injury of the left common carotid artery of 34 animals was performed. In 12 animals, polymer matrixes containing tyrphostin-47 were wrapped around the injured arteries to provide prolonged drug delivery (estimated dosage 28 micrograms/kg/24 hr); in 10 animals a polymer matrix without tyrphostin-47 was implanted; and in 12 animals only balloon injury was performed. The mean neointimal cross-sectional areas, luminal areas, and intima/media ratios were not significantly different among animals receiving local treatment with tyrphostin-47, sham polymer after injury, or balloon injury without polymer implantation. We conclude that despite inhibition of smooth-muscle cell proliferation by tyrphostin-47 in vitro, sustained local delivery of this tyrosine kinase inhibitor does not result in a reduction of neointimal proliferation in the rat carotid injury model.

Animals↗