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T Meinertz

Publications and source records attributed to T Meinertz.

At least 37 records · Page 2Linked to original sources
PubMed2003

[Comparison of an edema-sensitive HASTE-TIRM sequence with delayed contrast enhancement in acute myocardial infarcts].

GOAL: Comparison between a fluid-sensitive (HASTE-TIRM)-sequence and delayed contrast-enhancement in patients with acute myocardial infarct (AMI) in MRI. MATERIAL AND METHODS: 32 patients with AMI were imaged 7 +/- 4 days after the time of infarction with a 1.5 T unit using a T2 HASTE-TIRM and a contrast-enhanced (CE) T1 turbo FLASH sequence. A threshold method (>2 SD in comparison with normal myocardium) was used to quantify the hyperintense zones in both sequences. The transmurality of the hyperintense regions was measured on a segmental basis. RESULTS: The hyperintense areas were larger on the HASTE-TIRM sequence with 29.6 +/- 13.2 % of the left ventricular (LV) area as compared to the CE-MRI with 19.2 +/- 10 % of the LV area (p < 0.0001). The measured transmurality was higher with the HASTE-TIRM sequence than with the CE-MRI (p < 0.0001). While the correlation between CE-MRI and peak creatine kinase (CK max) was good (r = 0.59, p < 0.001), no correlation was found between the HASTE-TIRM sequence and CK max (r = 0.29, p = ns). CONCLUSIONS: The peri-infarct edema can be depicted with a HASTE-TIRM sequence in addition to the non-viable infarct zone. The HASTE-TIRM sequence shows a higher transmurality of the hyperintense regions than the CE-MRI. The additional area depicted by the HASTE-TIRM sequence could represent functionally impaired but viable myocardium).

Adult↗
PubMed2002

[Percutaneous revascularization of multivessel coronary disease using stents - a multicenter, prospective study].

BACKGROUND AND OBJECTIVE: Symptomatic patients with multivessel coronary disease (MVD) benefit from both coronary artery bypass grafting (CABG) and percutaneous coronary angioplasty (PTCA). The >>German Angioplasty Bypass Investigation<< (GABI-I) trial randomized patients to one of these treatment strategies between 1986 and 1991. In order to evaluate the impact of current technology, in particular coronary stents, the GABI-II trial was initiated, which in 1996 and 1997 prospectively enrolled patients according to the initial GABI-I criteria. PATIENTS AND METHODS: Into the study 136 consecutive patients (108 men, 28 women; 63 +/- 12 years) were included. Patients from GABI-I served as controls. RESULTS: A mean of 2.1 +/- 0.5 vessels were treated per patient (vs. 1.9 +/- 0.5 vessels in the PTCA arm of GABI-I) and 63 % of the lesions were covered with stents. With respect to the primary endpoint less patients remained with a CCS class III or IV in GABI-II after 12 months (1,5 % vs. 8 % in the PTCA arm of GABI-I, p<0,01). No patient required emergency or urgent bypass operation in GABI-II (vs. 9 % in GABI-I, p < 0.01). After 12 months, 8 % of the patients were sent for bypass surgery (CABG) vs. 21 % in GABI-I (p < 0.001), and 20 % (vs. 23 % in GABI-I) of the patients underwent Re-PTCA. The percentage of patients without reinterventions was 72 % vs. 56 % in GABI-I (p < 0.01), but remained lower compared to patients randomized to CABG in GABI-I (94 %, p < 0.001). CONCLUSION: PTCA in patients with MVD is still associated with a higher reintervention rate as compared with CABG. However, in contrast to angioplasty a decade ago, PTCA in conjunction with stents significantly lowered the need for subsequent revascularization, which was mainly driven by the reduced necessity for bypass surgery.

Aged↗
PubMed2002

[Are the acute effects of transdermal estradiol in postmenopausal women with coronary disease related to changes of the autonomic tone?].

The single application of estradiol in postmenopausal women with symptomatic coronary heart disease has an antiischemic effect, which seems to be mainly related to the relaxation of the vascular smooth muscle. Longterm replacement with estrogen in postmenopausal women reduces their increased sympathetic activity. The aim of the double-blinded study was to assess whether a single transdermal estradiol administration also has an effect on the sympathovagal balance and may additionally explain the acute effects of estradiol. Methods Fifteen women with symptomatic and angiographically proven coronary artery disease were cross-over randomized to two 100-microgram patches of estradiol or identical placebo. After one week the women received the opposite treatment. One day after patch application a 24-hour Holter-ECG recording was performed to assess the mean heart rate over 24 hours as well as time domain and frequency domain indices of the heart rate variability. Results The estradiol plasma concentration rose significantly from 354 +/- 176 pmol/l after placebo to 800 +/- 260 pmol/l after estradiol application. Heart rate during placebo was 74 +/- 15 bpm and during therapy 74 +/- 15 bpm. Heart rate variability was not different for time domain indices such as SDNN (estradiol: 64 +/- 31 ms; placebo: 65 +/- 33 ms) or for frequency domain indices such as LF (estradiol: 15.8 +/- 8.0 ms; placebo: 15.3 +/- 9.4 ms) and HF (estradiol: 12.1 +/- 8.5 ms; placebo: 12.9 +/- 9.9 ms). Conclusion A single transdermal application of estradiol did not modify heart rate or heart rate variability of women with coronary artery disease. The modulation of the autonomic tone does not seem to be a relevant mechanism of short-term estradiol effects.

Administration, Cutaneous↗
PubMed2002

[Evaluation of infrequent episodes of palpitations with a patient-activated hand-held electrocardiograph].

UNLABELLED: The disadvantage of most devices presently available for cardiac rhythm event monitoring is that they require either permanently attached electrodes or the subcutaneous implantation of the device. The aim of the study was to evaluate the feasibility and diagnostic yield of a hand-held, portable electrocardiograph for the evaluation of infrequent episodes of palpitations. In contrast to other devices, this electrocardiograph records and stores the electrocardiograms with integral electrodes, which makes long-term attached electrodes not unnecessary. METHODS: The study included 55 consecutive patients with palpitations less than once a week. The patients received the electrocardiograph Miniscope MS-3 with integral tripod electrodes (Schiller AG, Switzerland) to record a one-channel electrocardiogram during a recurrent episode. The frequency of device activation and the atrial rhythm during an episode was assessed. RESULTS: Forty-one (75%) patients had at least one episode within 38 +/- 22 days. The first episode occurred within the first week in 18 cases, during the 2nd in 9, during the 3rd in 9, during the 4th in 2 patients, and in 3 patients between the 4th and 12th week. All episodes could be properly analyzed: Twenty-three patients had sinus rhythm, 7 paroxysmal atrial fibrillation, 7 paroxysmal atrial flutter, and 4 an AV node reentry tachycardia. Eleven of the 23 patients with sinus rhythm additionally had premature atrial or ventricular contractions. Mean heart rate was 111 +/- 45 bpm. A second episode was recorded in 22 and a third episode in 12 patients. All patients had during the subsequent episode the same cardiac rhythm as during their first episode. CONCLUSIONS: Patients evaluated for their infrequent palpitations had during event monitoring a recurrent episode in 75% that occurred in 88% within the first 4 weeks. All patients were able to activate the electrocardiograph and could store an electrocardiogram with the integral electrodes. Patient-activated event monitoring reliably identified patients with an atrial arrhythmia who need further invasive evaluation and treatment, and ruled out patients with sinus rhythm and premature contractions.

Adult↗
PubMed2002

Anaerobic threshold and maximal oxygen uptake in patients with coronary artery disease and stable angina before and after percutaneous transluminal coronary angioplasty.

In this study, we investigated the effect of percutaneous transluminal coronary angioplasty (PTCA) on functional exercise capacity, oxygen uptake at anaerobic threshold (VO(2 AT)) and maximal oxygen uptake (VO(2 max)) in patients with coronary artery disease (CAD). Twenty-five patients with CAD and stable angina pectoris underwent spiroergometry before and after PTCA. All patients had reduced functional capacity with Weber class B in 5, class C in 16 and class D in 4 patients with mean VO(2 AT) of 9.4 +/- 1.5 ml.kg(-1).min(-1) and mean VO(2 max) of 13.3 +/- 3.3 ml. kg(-1).min(-1). After PTCA, VO(2 max) (15.8 +/- 3.1 ml.kg(-1). min(-1)) increased significantly (p < 0.001) compared to before PTCA. Subgroup analysis revealed that patients with low functional capacity before PTCA (VO(2 max) <15 ml x kg(-1) x min(-1)) had the most benefit from PTCA with an increase in VO(2 AT) from 8.7 +/- 1.0 to 9.6 +/- 1.4 ml x kg(-1) x min(-1) (p < 0.05) and of VO(2 max) from 11.3 +/- 2.2 to 14.8 +/- 3.5 ml x kg(-1) x min(-1) (p < 0.001) whereas in patients with VO(2 max) >15 ml x kg(-1) x min(-1), VO(2 AT) (p = 0.9) and VO(2 max) (p = 0.2) did not improve significantly. In conclusion, there is reduced functional capacity and VO(2 max) which improved after PTCA in CAD patients. In patients with low VO(2 max) before PTCA, functional capacity, VO(2 AT) and VO(2 max) significantly improved after PTCA, suggesting reversible myocardial impairment induced by intermittent myocardial ischemia. Patients with higher VO(2 max) had no significant benefit from PTCA with respect to functional capacity, VO(2 max) and VO(2 AT).

Aged↗
PubMed2002

Prediction of left ventricular functional recovery by dobutamine echocardiography, F-18 deoxyglucose or 99mTc sestamibi nuclear imaging in patients with chronic myocardial infarction.

BACKGROUND: Currently, several modalities are available to predict viability, however, studies comparing various modalities validated by functional recovery after revascularization are scarce. This study analyzed the relative merits of low-dose dobutamine echocardiography, F-18 deoxyglucose (FDG) positron emission tomography (PET) and (99m)Tc sestamibi single-photon emission computed tomography to predict functional recovery after revascularization in patients with chronic myocardial infarction. METHODS: Patients with chronic coronary occlusion (duration: 3.1 +/- 4.8 years) and impaired left ventricular function (ejection fraction: 42 +/- 13%) underwent low-dose dobutamine echocardiography (20 microg/kg/min), FDG-PET and (99m)Tc sestamibi imaging before revascularization. Revascularization was performed irrespective of any viability data. Follow-up angiography was obtained 4.8 +/- 2.5 months after revascularization. RESULTS: Viability analysis was performed in 34 patients with patent target vessel at follow-up, of whom 9 (27%) exhibited functional recovery on left ventricular angiography. For dobutamine echocardiography, improvement of >/=2 adjacent akinetic segments resulted in improved sensitivity of 89% and specificity of 80% to predict functional recovery. For glucose metabolism, FDG uptake >55% was an optimal threshold yielding a sensitivity of 89% and a specificity of 68%. With respect to perfusion, (99m)Tc sestamibi uptake >60% was the best cutoff resulting in a sensitivity and a specificity of 56 and 88%, respectively. A concordant match of FDG >55% and of (99m)Tc sestamibi >50% resulted in optimized sensitivity (78%) and specificity (80%) with dual imaging. CONCLUSIONS: Recovery of chronically dysfunctional myocardium can be predicted with high accuracy by stimulation of contractile reserve or by concordant match of preserved glucose metabolism and residual perfusion.

Aged↗
PubMed2002

[Primary and secondary prevention of coronary heart disease: smoking].

Although smoking is one of the major risk factors for the development of atherosclerosis, the exact mechanism of smoking-related vascular disease is not known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systemic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating normal vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction in both conductance and resistance vessels. This effect seems to be dose-related and reversible. The mechanism of endothelial dysfunction in smokers is not known, but increased degradation of nitric oxide by oxygen-derived free radicals has been suggested. In addition, smoking could cause oxidative inactivation of tetrahydrobiopterin, a critical cofactor of nitric oxide, leading to an uncoupling of the endothelial nitric oxide synthase with increased superoxide production and decreased nitric oxide bioactivity. Other pro-atherosclerotic effects of smoking are discussed. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counseling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment.

Adolescent↗
PubMed2001

Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease.

BACKGROUND: Endothelial function is impaired in coronary artery disease and may contribute to its clinical manifestations. Increased oxidative stress has been linked to impaired endothelial function in atherosclerosis and may play a role in the pathogenesis of cardiovascular events. This study was designed to determine whether endothelial dysfunction and vascular oxidative stress have prognostic impact on cardiovascular event rates in patients with coronary artery disease. METHODS AND RESULTS: Endothelium-dependent and -independent vasodilation was determined in 281 patients with documented coronary artery disease by measuring forearm blood flow responses to acetylcholine and sodium nitroprusside using venous occlusion plethysmography. The effect of the coadministration of vitamin C (24 mg/min) was assessed in a subgroup of 179 patients. Cardiovascular events, including death from cardiovascular causes, myocardial infarction, ischemic stroke, coronary angioplasty, and coronary or peripheral bypass operation, were studied during a mean follow-up period of 4.5 years. Patients experiencing cardiovascular events (n=91) had lower vasodilator responses to acetylcholine (P<0.001) and sodium nitroprusside (P<0.05), but greater benefit from vitamin C (P<0.01). The Cox proportional regression analysis for conventional risk factors demonstrated that blunted acetylcholine-induced vasodilation (P=0.001), the effect of vitamin C (P=0.001), and age (P=0.016) remained independent predictors of cardiovascular events. CONCLUSIONS: Endothelial dysfunction and increased vascular oxidative stress predict the risk of cardiovascular events in patients with coronary artery disease. These data support the concept that oxidative stress may contribute not only to endothelial dysfunction but also to coronary artery disease activity.

Antioxidants↗
PubMed2001

Beneficial effects of alpha-lipoic acid and ascorbic acid on endothelium-dependent, nitric oxide-mediated vasodilation in diabetic patients: relation to parameters of oxidative stress.

The impairment of nitric oxide (NO)-mediated vasodilation in diabetes has been attributed to increased vascular oxidative stress. Lipoic acid has been shown to have substantial antioxidative properties. The aim of this study was to assess the effect of lipoic acid on NO-mediated vasodilation in diabetic patients in comparison with the well-recognized effect of ascorbic acid. Using venous occlusion plethysmography, we examined the effects of lipoic acid (0.2 mM) and ascorbic acid (1 and 10 mM) on forearm blood flow responses to acetylcholine, sodium nitroprusside and concomitant infusion of the NO-inhibitor, N(G)-monomethyl-L-arginine, in 39 diabetic patients and 11 control subjects. Plasma levels of antioxidants and parameters of lipid peroxidation were measured and correlated to endothelial function tests. Lipoic acid improved NO-mediated vasodilation in diabetic patients, but not in controls. NO-mediated vasodilation was improved by ascorbic acid at 10 mM, but not 1 mM. Improvements of endothelial function by ascorbic acid and lipoic acid were closely related. The beneficial effects of lipoic acid were positively related to plasma levels of malondialdehyde and inversely related to levels of ubiquinol-10. These findings support the concept that oxidative stress contributes to endothelial dysfunction and suggest a therapeutic potential of lipoic acid particularly in patients with imbalance between increased oxidative stress and depleted antioxidant defense.

Acetylcholine↗
PubMed2001

Antibodies to chlamydial lipopolysaccharides in unstable angina pectoris.

Patients with coronary artery disease frequently have elevated antibody titers against Chlamydia pneumoniae, but whether antichlamydial antibody titers are correlated with prognosis in unstable angina remains unclear. We therefore investigated the sera of 1,096 patients with unstable angina regarding immunoglobulin (Ig) IgG, IgA, and IgM antibody titers against chlamydial lipopolysaccharides (LPS) and the concentrations of C-reactive protein (CRP) and troponin T (TnT). Anti-LPS IgG titers were increased in 45% of patients at enrollment and in 48% of patients at discharge (p <0.0001). Anti-LPS IgA titers were increased in 27% of patients at enrollment and in 33% of patients at discharge (p <0.0001). Patients who subsequently died had significantly lower IgM titers at enrollment than patients without events (p = 0.016). IgG, IgA, or IgM titers did not correlate with concentrations of CRP or TnT. In this large-scale study of patients with unstable angina, we frequently found elevated antichlamydial antibody titers. Patients with low IgM anti-LPS titers were at risk for subsequent death. However, there was no correlation between antichlamydial antibody titers and CRP or TnT.

Aged↗
PubMed2001

Effects of in vivo nitroglycerin treatment on activity and expression of the guanylyl cyclase and cGMP-dependent protein kinase and their downstream target vasodilator-stimulated phosphoprotein in aorta.

BACKGROUND: Chronic in vivo treatment with nitroglycerin (NTG) induces tolerance to nitrates and cross-tolerance to nitrovasodilators and endothelium-derived nitric oxide (NO). We previously identified increased vascular superoxide formation and reduced NO bioavailability as one causal mechanism. It is still controversial whether intracellular downstream signaling to nitrovasodilator-derived NO is affected as well. METHODS AND RESULTS: We therefore studied the effects of 3-day NTG treatment of rats and rabbits on activity and expression of the immediate NO target soluble guanylyl cyclase (sGC) and on the cGMP-activated protein kinase I (cGK-I). Tolerance was induced either by chronic NTG infusion via osmotic minipumps (rats) or by NTG patches (rabbits). Western blot analysis, semiquantitative reverse transcription-polymerase chain reaction, and Northern blot analysis revealed significant and comparable increases in the expression of sGC alpha(1) and beta(1) subunit protein and mRNA. Studies with the oxidative fluorescent dye hydroethidine revealed an increase in superoxide in the endothelium and smooth muscle. Stimulation with NADH increased superoxide signals in both layers. Although cGK-I expression in response to low-dose NTG was not changed, a strong reduction in vasodilator-stimulated phosphoprotein (VASP) serine239 phosphorylation (specific substrate of cGK-I) was observed in tolerant tissue from rats and rabbits. Concomitant in vivo and in vitro treatment with vitamin C improved tolerance, reduced oxidative stress, and improved P-VASP. CONCLUSIONS: We therefore conclude that increased expression of sGC in the setting of tolerance reflects a chronic inhibition rather than an induction of the sGC-cGK-I pathway and may be mediated at least in part by increased vascular superoxide.

Administration, Cutaneous↗
PubMed2001

Mechanisms underlying endothelial dysfunction in diabetes mellitus.

Incubation of endothelial cells in vitro with high concentrations of glucose activates protein kinase C (PKC) and increases nitric oxide synthase (NOS III) gene expression as well as superoxide production. The underlying mechanisms remain unknown. To address this issue in an in vivo model, diabetes was induced with streptozotocin in rats. Streptozotocin treatment led to endothelial dysfunction and increased vascular superoxide production, as assessed by lucigenin- and coelenterazine-derived chemiluminescence. The bioavailability of vascular nitric oxide (as measured by electron spin resonance) was reduced in diabetic aortas, although expression of endothelial NOS III (mRNA and protein) was markedly increased. NOS inhibition with N:(G)-nitro-L-arginine increased superoxide levels in control vessels but reduced them in diabetic vessels, identifying NOS as a superoxide source. Similarly, we found an activation of the NADPH oxidase and a 7-fold increase in gp91(phox) mRNA in diabetic vessels. In vitro PKC inhibition with chelerythrine reduced vascular superoxide in diabetic vessels, whereas it had no effect on superoxide levels in normal vessels. In vivo PKC inhibition with N:-benzoyl-staurosporine did not affect glucose levels in diabetic rats but prevented NOS III gene upregulation and NOS-mediated superoxide production, thereby restoring vascular nitric oxide bioavailability and endothelial function. The reduction of superoxide in vitro by chelerythrine and the normalization of NOS III gene expression and reduction of superoxide in vivo by N:-benzoyl-staurosporine point to a decisive role of PKC in mediating these phenomena and suggest a therapeutic potential of PKC inhibitors in the prevention or treatment of vascular complications of diabetes mellitus. The full text of this article is available at http://www.circresaha.org.

Animals↗