PubMed Health⌕ Search

Biomedical subjects

G Nickenig

Publications and source records attributed to G Nickenig.

At least 19 recordsLinked to original sources
PubMed2006

[Pharmacotherapy of supraventricular arrhythmias. What comes, what remains, what goes?].

Supraventricular tachycardias consist of AV-nodal-reentrant-tachycardias, atrioventricular tachycardias with accessory pathways (WPW-syndrome), atrial tachycardias, atrial fibrillation and atrial flutter. Only specific ECG interpretation with an exact arrhythmia classification offers the way to perform modern differential therapy including drug treatment and also interventional therapy modalities. In atrial fibrillation, drug treatment is still first-line therapy: physicians have to make a decision either to follow the rate or rhythm control concept. In case of rhythm control, drug therapy is tailored to the individual patient taking into account the patients symptomatology, left ventricular ejection fraction and nature and degree of an underlying cardiac disease. Drug refractory symptomatic atrial fibrillation patients should be considered for interventional treatment like pulmonary vein ablation. Recurrent typical right atrial flutter, AV-nodal-reentrant-tachycardia and all forms of atrioventricular tachycardias however are indications for catheter ablation; long-term drug treatment will only be performed in rare cases.

Anti-Arrhythmia Agents↗
PubMed2006

[Ventricular tachycardia. Diagnostic spectrum and therapeutic measures].

The origin of ventricular tachycardia lies in the ventricular tissue and includes a variety of symptoms such as monomorphic and polymorphic ventricular tachyarrhythmia (VT), ventricular flutter and ventricular fibrillation. Due to transitions of one form of VT to another, any form of VT incurs in principal the risk of cardiac failure. Apart from different electrophysiologic mechanisms such as reentry or triggered activity, any occurrence of VT has to be considered in an individual context: VT can be caused by structural heart disease such as coronary artery disease or dilative cardiomyopathy, or primary electrical disease such as long or short QT syndromes or can even occur without any detectable cause (idiopathic VT). Correct identification of the underlying cause of the arrhythmia is essential for the prognosis, differential therapy and long-term treatment of patients.

Catheter Ablation↗
PubMed2005

Comparative study of tacrolimus and paclitaxel stent coating in the porcine coronary model.

BACKGROUND: Tacrolimus is a potent antiproliferative and immunosuppressive agent allowing for improved endothelial regeneration. The aim of our study was the preclinical evaluation of tacrolimus in a drug eluting nonerodable polymer stent system and its comparison with paclitaxel. METHODS AND RESULTS: A total of 40 domestic pigs and 10 mini-pigs underwent coronary stenting with a follow-up time between 6 hours and 3 months. Stents were implanted in coronary arteries with an overstretch ratio of 1.2. After 3 days, a 1.73 microg/mm(2) coating produced tacrolimus tissue levels of 20 mumol/l in the coronary artery wall. Effective tissue concentrations were sustained for 28 days. Based on histomorphometric analysis, tacrolimus stent treated vessels had a reduced extent of neointima formation compared with controls at 28 days (-51% compared to control) but not at 3 months. High dose paclitaxel stent coating (1.44 microg/mm(2)) was complicated by unexpected deaths of pigs and thrombotic stent occlusion at control angiography. Long-term porcine data showed no persistent inhibition of neointimal growth by paclitaxel and tacrolimus stent coating. CONCLUSIONS: Similar to paclitaxel, tacrolimus stent coating reduces neointimal proliferation in the porcine coronary model. However, dosing and long-term efficacy remains a critical issue in stent-based local drug delivery.

Animals↗
PubMed2004

Does statin therapy influence steroid hormone synthesis?

Statins reduce cholesterol and isoprenoid de novo biosynthesis as well as receptor mediated uptake of cholesterol for steroidogenesis. The present randomized placebo-controlled trial investigated whether pravastatin (40 mg/day) reduces the plasma concentrations of steroid hormones as well as of gonadotropins. Patients (n = 22; 15 males, 7 females) were treated with pravastatin (40 mg/day) or placebo. Levels of total and LDL cholesterol, the steroid hormones estradiol, testosterone, cortisol and dehydroepiandrosterone sulphate (DHEAS) as well as FSH and LH were studied. Pravastatin led to a significant reduction of total cholesterol and LDL cholesterol. There was no significant change in estradiol, testosterone, cortisol or DHEAS plasma concentrations. There was no compensatory change in FSH or LH. It is concluded that pravastatin does not alter steroid hormones or gonadotropins in a clinically applicable dose, which significantly reduces total and LDL cholesterol.

Aged↗
PubMed2004

Beneficial effects of statins in patients with non-ischemic heart failure.

OBJECTIVE: HMG CoA reductase inhibitors (statins) may exert a wide array of cholesterol independent effects including antihypertrophic effects on the heart. Their role in the treatment of heart failure has not been studied. METHODS AND RESULTS: 15 patients with heart failure NYHA II-III based on non-ischemic dilated cardiomyopathy were randomized in a double-blind study to 0.4 mg cerivastatin or placebo for an average treatment period of 20 weeks. Quality of life and exercise capacity increased significantly in the statin treatment but not in the placebo group (Minnesota Living with Heart Failure Questionnaire, 6 min walking test). Concomitantly, there was a trend towards increased left ventricular ejection fraction (radionuclear ventriculography) and improved endothelial function (forearm blood flow). Statins decreased plasma concentrations of troponine T, high sensitive C-reactive protein (hsCRP), plasminogen activator inhibitor-1 (PAI-1) and tumor necrosis factor alpha (TNFalpha). CONCLUSIONS: Statins induce beneficial effects in patients with non-ischemic cardiomyopathy leading to improvement of quality of life and exercise capacity disclosing a promising novel treatment strategy for patients with heart failure.

Anticholesteremic Agents↗
PubMed2003

[Detection of left ventricular ischemia at rest by tissue Doppler echocardiography].

UNLABELLED: A 53-year old woman without a previous history of cardiac disease was successfully resuscitated from ventricular fibrillation. Despite a normal two dimensional echocardiogram, tissue Doppler analysis of left ventricular long-axis contraction revealed marked postsystolic contractions in the territory of the left coronary artery suggesting ischemia as the underlying pathogenetic mechanism. This was confirmed by coronary angiography which revealed a high-grade ostial stenosis of the left main stem. After coronary artery bypass surgery, the tissue Doppler findings normalized. CONCLUSION: Assessment of regional long axis function by tissue Doppler echocardiography may yield important additional findings even if two-dimensional echocardiography is apparently normal.

Coronary Angiography↗
PubMed2003

Atorvastatin stent coating does not reduce neointimal proliferation after coronary stenting.

PURPOSE: Statins seem to be suitable for restenosis prevention via reduction of smooth muscle cell proliferation, anti-inflammatory effects, and improvement of endothelial function. The aim of the present study was to test the efficacy of an atorvastatin stent coating for restenosis inhibition in the porcine coronary stent model. METHODS AND RESULTS: Twenty stents (BiodivYsio Matrix LO, uncoated or with 56 microg atorvastatin load) were implanted in LAD and CX coronary arteries of 10 domestic pigs with an over stretch ratio of 1.25. Quantitative angiography and histomorphometry of the stented arteries asserted statistic equality of the baseline parameters between the control and treatment group. After 28 days, there was no significant difference in parameters describing in-stent restenosis (neointimal area 3.14 +/- 1.13 mm(2) [control] vs. 3.12 +/- 1.07 mm(2) [atorvastatin stent]; p = 0.978). However, there was a trend towards a lower degree of inflammation in the atorvastatin stent group. CONCLUSION: Atorvastatin stent coating showed a trend towards reduced local inflammation near the stent struts, but could not reduce neointimal formation in the porcine coronary over stretch model.

Administration, Topical↗
PubMed2002

[Coronary-subclavian steal syndrome].

HISTORY AND CLINICAL FINDINGS: A-46-year-old woman with generalized atherosclerosis and coronary triple vessel disease was admitted with recurrent angina pectoris 17 months after primarily successful triple coronary artery bypass grafting (CABG). The symptoms were induced by exercise of the arms, e. g. carrying shopping bags in the left hand. INVESTIGATIONS: Stress technetium scans showed pronounced left ventricular ischemia of the anterior wall and apex during left upper limb exercise in comparison to bicycle exercise. The coronary angiography showed reverse flow in the internal mammary artery (IMA) graft to the left anterior descending artery (LAD), and aortography disclosed blockage of the proximal left subclavian artery. TREATMENT AND COURSE: : The patient declined percutaneous transluminal interventions or surgical procedures of the left subclavian artery. Because of mild angina and the lack of neurological symptoms, she was discharged on optimal drug treatment. CONCLUSION: : Patients with recurrence of cardiac symptoms after CABG surgery and IMA graft may have a coronary-subclavian steal syndrome. Clinically, these patients present with arterial blood pressure differences between left and right arm of typically more than 20 mmHg. The therapy of choice are percutaneous transluminal revascularization procedures of the subclavian artery.

Coronary Artery Bypass↗
PubMed2002

Central role of the AT(1)-receptor in atherosclerosis.

The renin-angiotensin system plays a major role in the pathogenesis of atherosclerosis. Most known effects of angiotensin II are mediated via activation of the AT(1)-receptor, which is in turn influenced to a great degree by levels of expression of the AT(1)-receptor. AT(1)-receptor activation is not only involved in vasoconstriction, water and salt homoeostasis and control of other neurohumoral systems, but also induces reactive oxygen species production, cellular hypertrophy and hyperplasia and apoptosis. Expression of this G-protein-coupled receptor is regulated by multiple factors. Among other conditions, oestrogen deficiency and hypercholesterolaemia increase AT(1)-receptor expression. Experimental data suggest that this augments the actions of angiotensin II, contributes to endothelial dysfunction, increases vascular production of reactive oxygen species, and via these mechanisms promotes atherosclerosis. Because of this, AT(1)-receptor regulation is likely to be critical in the development and progression of vascular lesions. Interventional studies demonstrated that ACE inhibitors which reduce AT(1)-receptor activation, improve endothelial dysfunction and inhibit onset and progression of atherosclerosis. The more specific AT(1)-receptor antagonists have also been shown to decrease blood pressure, protect renal function and to improve endothelial function. Thus, there is compelling evidence that AT(1)-receptor activation participates in the pathogenesis of atherosclerosis, and more importantly, that treatment regimens aiming at inhibition of AT(1)-receptor activation are promising anti-atherosclerotic therapeutic options.

Arteriosclerosis↗
PubMed2001

Endothelial dysfunction and oxidative stress during estrogen deficiency in spontaneously hypertensive rats.

BACKGROUND: Postmenopausal estrogen deficiency is associated with an increased cardiovascular risk, hypertension, and oxidative stress. Angiotensin type 1 (AT(1)) receptor regulation is involved in the pathogenesis of atherosclerosis. To characterize vascular function, oxidative stress, and AT(1) receptor regulation during estrogen deficiency, ovariectomized spontaneously hypertensive rats (SHR) were investigated in comparison with sham-operated animals and with ovariectomized rats receiving estrogen replacement therapy with 17beta-estradiol. METHODS AND RESULTS: Arterial blood pressure was similar in all 3 groups investigated. Five weeks after ovariectomy, endothelial dysfunction in aortic rings was observed, which was reversed by estrogen replacement therapy. Estrogen deficiency led to an enhanced vasoconstriction by angiotensin II. Vascular superoxide production was significantly increased compared with that in sham-operated rats, as measured by lucigenin chemiluminescence assays. Estrogen substitution normalized the production of free radicals in the vessel wall. Vascular AT(1) receptor expression was significantly upregulated by estrogen deficiency, as shown by quantitative reverse transcription-polymerase chain reaction, whereas endothelial NO synthase mRNA expression and NO release were unchanged. Five-week treatment of the animals with the AT(1) receptor antagonist irbesartan prevented endothelial dysfunction in ovariectomized rats and normalized the vascular production of free radicals. CONCLUSIONS: In SHR, estrogen deficiency leads to increased vascular free radical production and enhanced angiotensin II-induced vasoconstriction via increased vascular AT(1) receptor expression, resulting in endothelial dysfunction. Estrogen replacement therapy and AT(1) receptor antagonism prevent these pathological changes. Therefore, estrogen deficiency-induced AT(1) receptor overexpression and oxidative stress may play an important role in cardiovascular diseases associated with menopause.

Angiotensin II↗
PubMed2001

Prospective crossover comparison of carvedilol and metoprolol in patients with chronic heart failure.

OBJECTIVES: This study investigates the effects of a change of beta-adrenergic blocking agent treatment from metoprolol to carvedilol and vice versa in patients with heart failure (HF). BACKGROUND: Beta-blockers improve ventricular function and prolong survival in patients with HF. It has recently been suggested that carvedilol has more pronounced effects on left ventricular ejection fraction (LVEF) compared with metoprolol. It is uncertain whether a change from one beta-blocker to the other is safe and leads to any change of left ventricular function. METHODS: Forty-four patients with HF due to ischemic (n = 17) or idiopathic cardiomyopathy (n = 27) that had responded well to long-term treatment with either metoprolol (n = 20) or carvedilol (n = 24) were switched to an equivalent dose of the respective other beta-blocker. Before and six months after crossover of treatment, echocardiography, radionuclide ventriculography and dobutamine stress echocardiography were performed. RESULTS: Six months after crossover of beta-blocker treatment, LVEF had further improved with both carvedilol and metoprolol (carvedilol: 32 +/- 3% to 36 +/- 4%; metoprolol: 27 +/- 4% to 30 +/- 5%; both p < 0.05 vs. baseline), without interindividual differences. There were no changes in either New York Heart Association functional class or any other hemodynamic parameters at rest. Dobutamine stress echocardiography revealed a more pronounced increase of heart rate after dobutamine infusion in metoprolol- compared with carvedilol-treated patients. After dobutamine infusion, LVEF increased in the carvedilol- but not in the metoprolol-treated group. CONCLUSIONS: When switching treatment from one beta-blocker to the other, improvement of LVEF in patients with HF is maintained. Despite similar long-term effects on hemodynamics at rest, beta-adrenergic responsiveness is different in both treatments.

Adrenergic beta-Antagonists↗
PubMed2001

Reduction of oxidative stress and AT1 receptor expression by the selective oestrogen receptor modulator idoxifene.

1. The beneficial vasoprotective effects of oestrogens are hampered by their side effects on secondary sexual organs. Selective oestrogen receptor modulators (SERM) such as idoxifene may exert beneficial vascular effects without influencing cancerogenesis in breast or uterus. 2. In order to investigate vascular effects of selective oestrogen receptor modulators, we examined the impact of idoxifene on production of reactive oxygen species as well as AT1 receptor expression in vascular smooth muscle cells (VSMC). 3. Idoxifene caused a concentration- and time-dependent down-regulation of AT1 receptor mRNA expression, as assessed by Northern analysis. The maximal effect was reached with 10 micromol l(-1) idoxifene after a 4 h incubation period (33+/-7% of control levels). Western blots showed a similar down-regulation of AT1 receptor protein to 36+/-11% of control levels. 4. Confocal laserscanning microscopy using the redox sensitive marker 2',7'-dichlorofluorescein (DCF) and measurement of NAD(P)H oxidase activity in cell homogenates revealed that idoxifene effectively blunted the angiotensin II-induced production of reactive oxygen species. 5. In order to investigate the signal transduction involved in SERM-induced modulation of AT1 receptor expression, VSMC were preincubation with PD98059, genistein, wortmannin, or N(omega)-Nitro-L-arginine. The results suggested that idoxifene caused AT1 receptor down-regulation through nitric oxide-dependent pathways. 6. In conclusion, idoxifene reduces angiotensin II-evoked oxidative stress in VSMC. This could in part be explained by idoxifene-induced down-regulation of AT1 receptor expression. These results demonstrate that the selective oestrogen receptor modulator idoxifene may exert beneficial vascular effects which could be useful for therapeutic regimen in postmenopausal women at risk for cardiovascular diseases.

Angiotensin Receptor Antagonists↗