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1.  Immediate and 12 months follow up of function and lead integrity after cranial MRI in 356 patients with conventional cardiac pacemakers 
Conventional cardiac pacemakers are still often regarded as a contraindication to magnetic resonance imaging (MRI). We conducted this study to support the hypothesis that it is safe to scan patients with cardiac pacemakers in a 1.5 Tesla MRI, if close supervision and monitoring as well as adequate pre- and postscan programming is provided.
We followed up 356 patients (age 61.3 ± 9.1 yrs., 229 men) with single (n = 132) or dual chamber (n = 224) cardiac pacemakers and urgent indication for a cranial MRI for 12 months. The scans were performed at 1.5T. During the scan patients were monitored with a 3-lead ECG and pulse oximetry. Prior to the scan pacemakers were programmed according to our own protocol.
All 356 scans were completed without complications. No arrhythmias were induced, programmed parameters remained unchanged. No pacemaker dysfunction was identified. Follow-up examinations were performed immediately, 2 weeks, 2, 6, and 12 months after the scan. There was no significant change of pacing capture threshold (ventricular 0.9 ± 0.4 V@0.4 ms, atrial 0.9 ± 0.3 V@0.4 ms) immediately (ventricular 1.0 ± 0.3 V@0.4 ms, atrial 0.9 ± 0.4 V@0.4 ms) or at 12 months follow-up examinations (ventricular 0.9 ± 0.2 V@0.4 ms, atrial 0.9 ± 0.3 V@0.4 ms). There was no significant change in sensing threshold (8.0 ± 4.0 mV vs. 8.1 ± 4.2 mV ventricular lead, 2.0 ± 0.9 mV vs. 2.1 ± 1.0 mV atrial lead) or lead impedance (ventricular 584 ± 179 Ω vs. 578 ± 188 Ω, atrial 534 ± 176 Ω vs. 532 ± 169 Ω) after 12 months.
This supports the evidence that patients with conventional pacemakers can safely undergo cranial MRI in a 1.5T system with suitable preparation, supervision and precautions. Long term follow-up did not reveal significant changes in pacing capture nor sensing threshold.
PMCID: PMC4053551  PMID: 24903354
Pacemaker; Magnetic resonance imaging; Safety
2.  Circulating concentrations of GLP-1 are associated with coronary atherosclerosis in humans 
GLP-1 is an incretine hormone which gets secreted from intestinal L-cells in response to nutritional stimuli leading to pancreatic insulin secretion and suppression of glucagon release. GLP-1 further inhibits gastric motility and reduces appetite which in conjunction improves postprandial glucose metabolism. Additional vasoprotective effects have been described for GLP-1 in experimental models. Despite these vasoprotective actions, associations between endogenous levels of GLP-1 and cardiovascular disease have yet not been investigated in humans which was the aim of the present study.
GLP-1 serum levels were assessed in a cohort of 303 patients receiving coronary CT-angiography due to typical or atypical chest pain.
GLP-1 was found to be positively associated with total coronary plaque burden in a fully adjusted model containing age, sex, BMI, hypertension, diabetes mellitus, smoking, triglycerides, LDL-C (low density lipoprotein cholesterol), hsCRP (high-sensitive C-reactive protein), and eGFR (estimated glomerular filtration rate) (OR: 2.53 (95% CI: 1.12 – 6.08; p = 0.03).
Circulating GLP-1 was found to be positivity associated with coronary atherosclerosis in humans. The clinical relevance of this observation needs further investigations.
PMCID: PMC3765863  PMID: 23953602
GLP-1; Atherosclerosis; Coronary CT angiography
3.  SPECT myocardial perfusion imaging as an adjunct to coronary calcium score for the detection of hemodynamically significant coronary artery stenosis 
Coronary artery calcifications (CAC) are markers of coronary atherosclerosis, but do not correlate well with stenosis severity. This study intended to evaluate clinical situations where a combined approach of coronary calcium scoring (CS) and nuclear stress test (SPECT-MPI) is useful for the detection of relevant CAD.
Patients with clinical indication for invasive coronary angiography (ICA) were included into our study during 08/2005-09/2008. At first all patients underwent CS procedure as part of the study protocol performed by either using a multidetector computed tomography (CT) scanner or a dual-source CT imager. CAC were automatically defined by dedicated software and the Agatston score was semi-automatically calculated. A stress-rest SPECT-MPI study was performed afterwards and scintigraphic images were evaluated quantitatively. Then all patients underwent ICA. Thereby significant CAD was defined as luminal stenosis ≥75% in quantitative coronary analysis (QCA) in ≥1 epicardial vessel. To compare data lacking Gaussian distribution an unpaired Wilcoxon-Test (Mann–Whitney) was used. Otherwise a Students t-test for unpaired samples was applied. Calculations were considered to be significant at a p-value of <0.05.
We consecutively included 351 symptomatic patients (mean age: 61.2±12.3 years; range: 18–94 years; male: n=240) with a mean Agatston score of 258.5±512.2 (range: 0–4214). ICA verified exclusion of significant CAD in 66/67 (98.5%) patients without CAC. CAC was detected in remaining 284 patients. In 132/284 patients (46.5%) with CS>0 significant CAD was confirmed by ICA, and excluded in 152/284 (53.5%) patients. Sensitivity for CAD detection by CS alone was calculated as 99.2%, specificity was 30.3%, and negative predictive value was 98.5%. An additional SPECT in patients with CS>0 increased specificity to 80.9% while reducing sensitivity to 87.9%. Diagnostic accuracy was 84.2%.
In patients without CS=0 significant CAD can be excluded with a high negative predictive value by CS alone. An additional SPECT-MPI in those patients with CS>0 leads to a high diagnostic accuracy for the detection of CAD while reducing the number of patients needing invasive diagnostic procedure.
PMCID: PMC3527199  PMID: 23206557
Computed tomography coronary calcium scoring; Single photon emission computed tomography myocardial perfusion imaging; Invasive coronary angiography; Coronary artery disease
4.  MMP-1 serum levels predict coronary atherosclerosis in humans 
Myocardial infarction results as a consequence of atherosclerotic plaque rupture, with plaque stability largely depending on the lesion forming extracellular matrix components. Lipid enriched non-calcified lesions are considered more instable and rupture prone than calcified lesions. Matrix metalloproteinases (MMPs) are extracellular matrix degrading enzymes with plaque destabilisating characteristics which have been implicated in atherogenesis. We therefore hypothesised MMP-1 and MMP-9 serum levels to be associated with non-calcified lesions as determined by CT-angiography in patients with coronary artery disease.
260 patients with typical or atypical chest pain underwent dual-source multi-slice CT-angiography (0.6-mm collimation, 330-ms gantry rotation time) to exclude coronary artery stenosis. Atherosclerotic plaques were classified as calcified, mixed or non-calcified.
In multivariable regession analysis, MMP-1 serum levels were associated with total plaque burden (OR: 1.37 (CI: 1.02-1.85); p < 0.05) in a model adjusted for age, sex, BMI, classical cardiovascular risk factors, hsCRP, adiponectin, pericardial fat volume and medication. Specification of plaque morphology revealed significant association of MMP-1 serum levels with non-calcified plaques (OR: 1.16 (CI: 1.0-1.34); p = 0.05) and calcified plaques (OR: 1.22 (CI: 1,03-1.45); p < 0.05) while association with mixed plaques was lost in the fully adjusted model. No associations were found between MMP9 serum levels and total plaque burden or plaque morphology.
MMP-1 serum levels are associated with total plaque burden but do not allow a specification of plaque morphology.
PMCID: PMC2754422  PMID: 19751510
5.  Acute stent thrombosis in a sirolimus eluting stent after wasp sting causing acute myocardial infarction: a case report 
Cases Journal  2009;2:7800.
Hymenoptera venoms contain thrombogenic substances that might be responsible for cardiovascular events independent of anaphylactic reactions.
Case presentation
We report a 55-year-old man who experienced an acute ST-elevation myocardial infarction after wasp sting. The patient presented without signs of anaphylaxis or shock. The coronary angiography showed an acute stent thrombosis of the right coronary artery. Percutanous coronary intervention was performed immediately and this is an example for a cardiovascular complication associated with a hymenoptera sting, since the vasoactive, inflammatory, and thrombogenic substances of hymenoptera venoms potentially cause stent thrombosis and myocardial ischemia. To the best of our knowledge this is the first report of acute stent thrombosis in a sirolimus-eluting stent following hymenoptera sting.
Stent thrombosis is a possible complication after wasp sting induced by thrombogenic substances of the hymenoptera venom.
PMCID: PMC2769374  PMID: 19918484
6.  Low Adiponectin Levels Are an Independent Predictor of Mixed and Non-Calcified Coronary Atherosclerotic Plaques 
PLoS ONE  2009;4(3):e4733.
Atherosclerosis is the primary cause of coronary artery disease (CAD). There is increasing recognition that lesion composition rather than size determines the acute complications of atherosclerotic disease. Low serum adiponectin levels were reported to be associated with coronary artery disease and future incidence of acute coronary syndrome (ACS). The impact of adiponectin on lesion composition still remains to be determined.
Methodology/Principal Findings
We measured serum adiponectin levels in 303 patients with stable typical or atypical chest pain, who underwent dual-source multi-slice CT-angiography to exclude coronary artery stenosis. Atherosclerotic plaques were classified as calcified, mixed or non-calcified. In bivariate analysis adiponectin levels were inversely correlated with total coronary plaque burden (r = −0.21, p = 0.0004), mixed (r = −0.20, p = 0.0007) and non-calcified plaques (r = −0.18, p = 0.003). No correlation was seen with calcified plaques (r = −0.05, p = 0.39). In a fully adjusted multivariate model adiponectin levels remained predictive of total plaque burden (estimate: −0.036, 95%CI: −0.052 to −0.020, p<0.0001), mixed (estimate: −0.087, 95%CI: −0.132 to −0.042, p = 0.0001) and non-calcified plaques (estimate: −0.076, 95%CI: −0.115 to −0.038, p = 0.0001). Adiponectin levels were not associated with calcified plaques (estimate: −0.021, 95% CI: −0.043 to −0.001, p = 0.06). Since the majority of coronary plaques was calcified, adiponectin levels account for only 3% of the variability in total plaque number. In contrast, adiponectin accounts for approximately 20% of the variability in mixed and non-calcified plaque burden.
Adiponectin levels predict mixed and non-calcified coronary atherosclerotic plaque burden. Low adiponectin levels may contribute to coronary plaque vulnerability and may thus play a role in the pathophysiology of ACS.
PMCID: PMC2649379  PMID: 19266101

Results 1-6 (6)