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1.
Clin Res Cardiol ; 101(4): 297-303, 2012 Apr.
Article in English | MEDLINE | ID: mdl-22159895

ABSTRACT

BACKGROUND: Patients with patent foramen ovale (PFO) and cryptogenic stroke are at risk of recurrence. Therapeutic regimens range from no treatment to anticoagulation treatment to surgical or interventional closure. However, long-term follow-up is only available for up to 4 years. METHODS: Among ~5,000 transesophageal echocardiographies in stroke/TIA-patients between 1988 and 1997, a PFO was found and considered a possible mediator for the neurological event in 97 patients. In these patients, the PFO was judged to be responsible for the neurological event. Patients with cardiac or other reasons for embolism were excluded. The therapy for stroke was chosen by the attending physician. Follow-up information was obtained through telephone interviews. RESULTS: Follow-up was available for 86 patients (89%) with a mean period of 15.4 years (range, 11.2-25.9 years). Thirteen patients (15%) suffered from recurrent ischemic events (7 TIAs, 5 strokes, 1 peripheral embolism) after a mean period of 4.9 years. Four patients died, not associated with recurrent thromboembolism. The risk of recurrence was increased over the entire length of the mean follow-up period. The occurrence of recurrent events was not associated with differences in baseline data, the presence of ASA, PFO size or the chosen treatment. CONCLUSION: In patients with paradoxical embolism, recurrent ischemic events are frequent despite medical therapy. These events are not limited to the early years after the index event; this long-term follow-up revealed a risk of occurrence over the entire follow-up. These patients have a sustained risk of recurrence, requiring lifetime protection, which should be considered in tailoring individual therapeutic strategies.


Subject(s)
Embolism, Paradoxical/epidemiology , Foramen Ovale, Patent/complications , Stroke/epidemiology , Thromboembolism/epidemiology , Adult , Echocardiography, Transesophageal , Female , Follow-Up Studies , Humans , Ischemic Attack, Transient/epidemiology , Ischemic Attack, Transient/etiology , Male , Middle Aged , Recurrence , Risk Factors , Stroke/etiology , Thromboembolism/etiology , Time Factors
2.
Am J Cardiol ; 94(8): 1037-40, 2004 Oct 15.
Article in English | MEDLINE | ID: mdl-15476620

ABSTRACT

In this intravascular ultrasound study, the mechanism of restenosis after stenting in acute myocardial infarction (AMI) was investigated in 33 patients 6 months after primary coronary intervention for AMI. Restenosis after stenting for AMI was primarily caused by stent underexpansion, not by neointima formation.


Subject(s)
Coronary Restenosis/etiology , Myocardial Infarction/surgery , Postoperative Complications/etiology , Stents , Coronary Restenosis/diagnostic imaging , Female , Humans , Male , Middle Aged , Postoperative Complications/diagnostic imaging , Ultrasonography
3.
J Am Soc Echocardiogr ; 17(9): 954-61, 2004 Sep.
Article in English | MEDLINE | ID: mdl-15337960

ABSTRACT

OBJECTIVE: This study was performed to validate noninvasive transthoracic Doppler ultrasound (TTD) with simultaneous invasive Doppler guidewire measurements in patients after minimal invasive direct coronary artery bypass operation. METHODS: A total of 14 patients were examined 3 to 8 days after minimal invasive direct coronary artery bypass operation. TTD was performed to measure systolic and diastolic peak velocities of the left internal mammary artery (LIMA) at rest and during adenosine-induced hyperemia. Simultaneous Doppler guidewire measurements were performed. RESULTS: LIMA flow was detected in 12 of 14 patients (86%). There was high agreement between TTD and Doppler guidewire measurements of LIMA flow velocities (systolic peak velocity: r = 0.86, y = 11.3 + 0.82x +/- 7.9; diastolic peak velocity: r = 0.95, y = 5.7 + 1.02x +/- 7.5; average peak velocity: r = 0.95, y = 5.2 + 0.94x +/- 5.4; and flow velocity reserve: r = 0.97, y = 5.2 + 0.99x +/- 4.5). CONCLUSION: TTD represents an accurate method to evaluate flow velocities and flow velocity reserve of LIMA bypass grafts even in the early phase after minimal invasive direct coronary artery bypass operation.


Subject(s)
Coronary Artery Bypass , Echocardiography, Doppler , Internal Mammary-Coronary Artery Anastomosis , Mammary Arteries/diagnostic imaging , Adult , Aged , Blood Flow Velocity , Female , Humans , Male , Mammary Arteries/surgery , Middle Aged , Minimally Invasive Surgical Procedures
4.
Cardiology ; 97(1): 29-36, 2002.
Article in English | MEDLINE | ID: mdl-11893827

ABSTRACT

BACKGROUND: Experimental studies have shown an activation of the angiotensin-converting enzyme (ACE) system as a response to endothelial injury. Recent publications have elucidated the hypothesis that the ACE gene polymorphism may influence the level of late luminal loss after coronary stent implantation. It is still unclear whether the polymorphism of the angiotensin gene is a major predictor of the extent of neointimal hyperplasia. In this multicenter study, we therefore tested the relationship between the ACE gene polymorphism and the restenosis rate after coronary stent implantation. METHODS: As a substudy of the optimization with intracoronary ultrasound (ICUS) to reduce stent restenosis (OPTICUS) study, we analyzed ACE serum levels and the ACE gene polymorphism in 154 patients at 9 different centers. All patients underwent elective coronary stent implantation in a stenosis of a major coronary vessel. Balloon inflations were repeated until a satisfactory result was achieved in on-line quantitative coronary angiography or ICUS fulfilling the OPTICUS study criteria. After follow-up of 6 months, all patients underwent reangiography under identical projections as the baseline procedure. A blinded quantitative analysis of the initial procedure as well as the follow-up examinations were performed by an independent core laboratory. ACE gene polymorphism and ACE serum activity were measured at the 6-month follow-up in a double-blinded setting. RESULTS: With respect to the ACE gene polymorphism, there were three subgroups: DD genotype (48 patients), ID (83 patients) and II (23 patients). The subgroups did not differ in regard to age, gender, extent of coronary artery disease, stenosis length, initial degree of stenosis or degree of stenosis after stent implantation. In all, 39 patients (25.3%) had significant restenosis: 12 DD patients (25.0%), 18 ID patients (21.7%) and 9 II patients (39.1%) (odds ratio 2.164, 95% confidence interval 0.853-5.493). We obtained the following results for ACE serum levels: 0.53 micromol/l/s in the DD subgroup, 0.29 micromol/l/s in the ID subgroup and 0.09 micromol/l/s in the II subgroup (p < 0.001). Multivariate logistic regression analysis of the influence of ACE gene polymorphism on the restenosis rate after coronary stent implantation adjusted for lesion length (>12 mm), ACE inhibitor or hydroxymethylglutaryl coenzyme A reductase (CSE) inhibitor treatment, age, male gender, diabetes mellitus, hypertension, high cholesterol, family history, smoking and three-vessel disease did not uncover any statistic significance. CONCLUSIONS: In contrast to other study groups, we were unable to disclose that the DD polymorphism of the ACE gene was associated with a higher rate of restenosis after coronary stent implantation in this multicenter study. In addition, patients with higher ACE serum levels did not show a higher restenosis rate in this trial. We conclude that the pathogenesis of restenosis is a multifactorial process involving various genetic and nongenetic factors.


Subject(s)
Blood Vessel Prosthesis Implantation , Coronary Restenosis/genetics , Coronary Stenosis/surgery , Gene Deletion , Graft Occlusion, Vascular/genetics , Peptidyl-Dipeptidase A/genetics , Polymorphism, Genetic/genetics , Stents , Aged , Coronary Angiography , Coronary Restenosis/blood , Coronary Restenosis/diagnostic imaging , Coronary Stenosis/blood , Coronary Stenosis/diagnostic imaging , Double-Blind Method , Female , Graft Occlusion, Vascular/blood , Graft Occlusion, Vascular/diagnostic imaging , Humans , Male , Middle Aged , Peptidyl-Dipeptidase A/blood , Predictive Value of Tests
5.
Echocardiography ; 13(6): 599-608, 1996 Nov.
Article in English | MEDLINE | ID: mdl-11442974

ABSTRACT

Intravascular ultrasound (IVUS) imaging provides cross-sectional views of the vessel lumen; however, lumen measurements still rely on operator-dependent border delineation and time-consuming lumen tracings. We tested a new system for automated lumen border detection in IVUS images based on acoustic quantification of blood and vessel wall. In 10 rabbits, 29 segments of the aorta were imaged in vivo using a 2.9-Fr IVUS catheter. IVUS images were obtained during motorized pullbacks of aortic segments of 18 mm length. Automated measurements of lumen dimensions were compared to automated measurements of a second pullback through the same segment, lumen measurements derived from visual border tracings in IVUS images, and to quantitative angiography. The automated system showed good reproducibility: Correlations for repeated measurements of lumen area, maximal and minimal lumen diameters were r = 0.97, r = 0.91, and r = 0.93, respectively. Automated measurements also correlated well to visual image analysis (lumen area, r = 0.97; maximal lumen diameter, r = 0.89; minimal lumen diameter, r = 0.89) and to angiographic measurements (lumen area, r = 0.93; lumen diameter, r = 0.95). In 12% of the images, the automated system overestimated lumen dimensions because of weak wall signals in the presence of echolucent structures next to the wall. Signal artifacts from the IVUS catheter itself or strong blood backscatter resulted in lumen underestimation in 6% of the images. Over- and underestimation of lumen by the border detection system were often associated with eccentric catheter position. Thus, lumen measurements in vivo IVUS images can be performed using an automated border detection system based on acoustic quantification of blood and vessel wall. The system allows reproducible and accurate measurements of lumen area and diameters. (ECHOCARDIOGRAPHY, Volume 13, November 1996)

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