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Biomedical subjects

H M Hoffmeister

Publications and source records attributed to H M Hoffmeister.

At least 19 recordsLinked to original sources
PubMed2006

Aortic insufficiency due to a partial left-coronary aortic valve prolapse and the detection of two small interatrial jets after blunt thoracic trauma.

Aortic valve regurgitation due to blunt thoracic trauma is a rare complication. Autopsy studies have been shown that the aortic valve is the most often lacerated one among the heart valves. Actually, we describe a case of a 47 year old man with the signs of heart failure after a blunt thoracic trauma 2 months before caused by aortic insufficiency due to a partial left-coronary aortic valve prolapse. Furthermore, transthoracic and transesophageal echocardiography revealed two small jets between the left and the right atrium.

Aortic Valve Insufficiency↗
PubMed2004

Increased fibrin specificity and reduced paradoxical thrombin activation of the combined thrombolytic regimen with reteplase and abciximab versus standard reteplase thrombolysis.

In patients with acute myocardial infarction treated with thrombolytics, platelet activation as well as alterations of the hemostatic and fibrinolytic systems have been described favoring early infarct-related artery reocclusion. We investigated the effects of a newer thrombolytic regimen with half-dose double-bolus reteplase (2 x 5 IU, 20 patients) combined with abciximab versus full-dose reteplase (2 x 10 IU, 18 patients) on the fibrinolytic and the hemostatic system in patients with acute ST-segment elevation (in the electrocardiogram) myocardial infarction. The thrombolytic regimen with half-dose reteplase in combination with abciximab caused in vivo a lower systemic plasminemia and a lower paradoxical activation of the contact phase of the coagulation system (measured as activated factor XII); a lower paradoxical thrombin activation/generation; and a lesser extent of fibrinogen breakdown compared with the reteplase regimen. These results could be, at least in part, a possible explanation for the observed significantly lower rates of reinfarction until 7 days after enrollment and of recurrent ischemia in the combination group in the Global Use of Strategies to Open Occluded Coronary Arteries V (GUSTO V) trial.

Abciximab↗
PubMed2003

Insulin-like effect of low-dose leptin on glucose transport in Langendorff rat hearts.

BACKGROUND: In a murine myotube cell line (C 2 C 12 myotubes), leptin at low physiological concentrations (1 ng/ml) has been shown to stimulate glucose transport and glycogen synthesis. The aim of the present study was to test whether an analogous leptin effect on glucose transport is detectable in the heart. METHODS AND RESULTS: We used the isolated Langendorff rat heart preparation with hemodynamic function control. Using polymerase chain reaction (RT-PCR), a 346- and 375-base fragment indicative for the short and long leptin receptor isoform was detected in the rat heart. Glucose transport rates were calculated using equimolar double tracer perfusion with the non-metabolizable glucose analog 3-O-methylglucose (3-O-MG) and the non-transportable tracer mannitol and two-compartimental modeling. 3-O-MG uptake at a perfusate glucose concentration of 11 mM was measured over 15 minutes in control hearts, hearts perfused with insulin (10 mU/ml), leptin (1 ng/ml) or insulin (10 mU/ml) plus leptin (1 ng/ml; n = 8 in each group). The basal 3-O-MG transport rate of 0,7351 +/- 0,051 micro mol/min/g wet weight was increased 4.18 fold with insulin, 2.69 fold with leptin, and 4.2 fold with leptin plus insulin. Simultaneous monitoring of hemodynamic function revealed a minor and transient effect of leptin on left ventricular pressure, which was strongly augmented in coperfusion with insulin. CONCLUSIONS: The data suggest that leptin at low physiological concentrations is able to exert a partial insulin like effect on glucose uptake. We speculate that the effect might be mediated by both leptin receptor isoforms. This leptin effect is additive to the effect of insulin and might therefore contribute to the insulin independent basal glucose supply of the heart. It can not be completely excluded that the observed leptin effect on glucose transport is secondary to altered myocardial function.

Animals↗
PubMed2003

Benefical effects of reteplase in combination with abciximab: platelet/leukocyte interactions and coagulation system.

Pathophysiological aspects of acute myocardial infarction include altered hemostatic and fibrinolytic systems as well as platelet activation. Treatment with thrombolytics and GP IIb/IIIa antagonists has been described as having an additional influence on these systems. We investigated the effects of a new thrombolytic regimen with half-dose double-bolus reteplase (2 x 5 IU, 20 patients) combined with abciximab versus full dose reteplase (2 x 10 IU, 18 patients) on platelet-granulocyte complexes and on thrombin-antithrombin III complexes in patients with acute ST-segment elevation myocardial infarction. In vivo, the thrombolytic regimen with half-dose reteplase in combination with abciximab caused fewer platelet-granulocyte aggregates (measured as percentage of CD41-positive granulocytes) and a lower paradoxical activation of the coagulation system (measured as thrombin-antithrombin III complex) compared with the reteplase regimen. The combination regimen could therefore have benefical effects on platelet-induced leukocyte activation and leukocyte-mediated proinflammatory/cytotoxic effects as well as on granulocyte-induced effects on endothelium, tissue damage and coagulation. This could be, at least in part, a possible explanation for the significantly lower rates of reinfarction, recurrent ischaemia and percutaneous coronary interventions observed during the early phase after an acute myocardial infarction in the combination group in the GUSTO-V trial.

Abciximab↗
PubMed2002

Influence of ACE inhibition on myocardial damage, the Kallikrein-Kinin system and hemostasis during cardiopulmonary bypass surgery.

BACKGROUND: ACE inhibitors may have a cardioprotective effect by enhancing bradykinin levels during cardiopulmonary bypass (CPB). However, ACE inhibition could lead to unwelcome effects on the kallikrein contact phase during CPB (since reduction of kallikrein activity by aprotinin has been shown to be beneficial) and may alter the hemostasis. We examined the effects of ACE inhibitors on intraoperative myocardial damage, kallikrein contact phase and hemostasis in patients undergoing CPB. METHODS: 47 patients randomly received either 20 mg/d enalapril or placebo. Creatine kinase (CK and CK-MB), lactate dehydrogenase (LDH), troponin T (TnT), thrombin-antithrombin III complex (TAT), fibrinogen and kallikrein-like activity were measured before surgery, during and immediately after CPB, at the end of surgery and 1, 3 and 5 days after surgery. RESULTS: No significant differences between enalapril- and placebo- treated patients concerning CK (318 +/- 38.6 U/l vs. 316 +/- 16.8 U/l), CK-MB, LDH, TnT (1.81 +/- 0.45 ng/ml vs. 1.52 +/- 0.34 ng/ml), TAT, fibrinogen and kallikrein-like-activity could be found during study period. CONCLUSIONS: Reduction of ischemic injury during CPB is not achieved with ACE inhibitors. However, treatment of patients with ACE inhibitors before and during CPB is fully feasible without side effects affecting the kallikrein contact phase or significant influence on hemostasis.

Administration, Oral↗
PubMed2001

The thrombolytic paradox.

Thrombolytic drugs do not only stimulate the plasmin system but also induce thrombin activation additionally to the preexisting hypercoagulative state in patients with acute myocardial infarction. Testing the in vitro-derived hypothesis of a plasmin-mediated activation of the contact phase of the coagulation leading to the procoagulant effect, several thrombolytic regimen have been evaluated. Paradoxical thrombin activation (referred to as "thrombolytic paradox") was related to absence of fibrin specificity. Highly fibrin-specific drugs like tenecteplase did not cause additional thrombin activation, while non-fibrin-specific drugs like streptokinase caused a marked additional activation of the contact phase and of thrombin. It could be shown that the thrombolytic paradox was related to the extent of systemic plasmin activation confirming the hypothesis of a plasmin-mediated factor XII/kallikrein system activation as cause of the thrombolytic paradox.

Fibrinolysin↗
PubMed2001

Percutaneous coronary interventions using a new 5 French guiding catheter: results of a prospective study.

The aim of this prospective study was to analyze the technical feasibility, the success rate, and the special complications of percutaneous coronary interventions (PCIs) using a newly released 5 Fr guiding catheter with an inner diameter of 0.058". The study was performed in 150 consecutive patients subjected to coronary angioplasty. In 89% of the patients, the intervention was started with a 5 Fr catheter (JR4 or JL4); in 16 patients a 6 or 7 Fr catheter was used because of unstable clinical conditions according to the decision of the interventional cardiologist. In 12 out of 134 patients, the guiding catheter had to be changed during the intervention from 5 Fr to a 6 or 7 Fr catheter due to poor backup support. In 112 out of 118 patients, the intervention was successfully performed using a 5 Fr catheter (95%); in 12 out of 16 patients, after changing the guiding catheter, the overall success rate was 93%. In patients with type A and B lesions who were initially treated using a 5 Fr catheter, the procedural success rate was 100% (81 out of 81), whereas in patients with type C lesions the procedural success rate was 83% (43 out of 53; P = 0.000053, Fisher's exact test). Furthermore, in patients with a diameter stenosis < 90%, the procedural success rate was 100% (57 out of 57), whereas in patients with a diameter stenosis of 90%-100%, the procedural success rate was 87% (67 out of 77; P = 0.0050). Stent implantation was performed successfully in 24 patients (18%) using the 5 Fr guiding catheter. This study confirms that PCI was technically feasible using a 5 Fr guiding catheter in the majority of consecutive patients with a success rate of 95%. There were significant differences in the success rate depending on the lesion type and the diameter stenosis. Complications were very rare and were not related to the guiding catheter. Limitations of the 5 Fr guiding catheters arose mainly from a poor backup support in long lesions and severe stenosis. Cathet Cardiovasc Intervent 2001;53:308-312.

Adult↗
PubMed2001

Subacute myocardial infarction: assessment by STIR T2-weighted MR imaging in comparison to regional function.

PURPOSE: Increased T2 signal intensity (SI) can be regularly observed in myocardial infarction. However, there are controversial reports about the relationship of elevated T2 SI to myocardial viability and some authors propose that high T2 SI serves as a sign of irreversible myocardial injury. This study investigates increased T2 SI compared to myocardial function in patients with reperfused subacute myocardial infarction. Preserved function was used as criterion for viability. METHODS: Ten healthy volunteers and 17 patients with myocardial infarction and patent infarct related coronary artery were examined on a 1.5 T Magnetom Vision system (Siemens). For T2-weighted MR imaging a breath-hold STIR sequence with dark-blood preparation was used. Cine FLASH 2D imaging was applied to assess myocardial function. Signal-to-noise (S/N) in STIR T2 images was measured in normal and infarcted regions and subsequently identified by two independent observers. Based on a 20 segment model of the left ventricle findings were compared to regional myocardial function. RESULTS: Elevated STIR T2 SI was found in all 17 patients and observed in 27% (204/754) of segments. S/N of normal myocardium was 5.1 +/- 0.7 in volunteers and 4.9 +/- 0.8 in patients (P = NS). Infarcted myocardium presented with significantly increased S/N 12.8 +/- 1.9 (P < 0.0001). Significant transmural elevation of T2 SI was noted in 32% of segments with preserved systolic function. CONCLUSION: Increased STIR T2 SI can be observed transmurally in post-ischemic myocardial regions with preserved function. It therefore cannot be used as an exclusive marker for the non-viable region.

Aged↗
PubMed2001

[Markers for the prognosis of success of coronary interventions: focus on changes in fibrinolysis and hemostasis].

BACKGROUND: The morphology of the culprit coronary lesion is a most important factor for the prognosis of a percutaneous coronary intervention in patients with acute coronary syndrome. The most widely accepted grading of the complexity of the coronary stenosis is the modified ACC/AHA grading (from A to C). DISTURBANCES OF FIBRINOLYTIC SYSTEM: Further alterations like a hypercoagulative state and a disturbed fibrinolytic system are known in patients with unstable angina pectoris. In these patients a close correlation was observed between the complexity of stenosis morphology and the disturbances in the fibrinolytic system judged as measurement of the tissue-type plasminogen activator mass concentration or as measurement of the activity of the plasminogen activator inhibitor (PAI-1). For markers of thrombin activation no close correlation to the morphological grading was found. CONCLUSION: It should be investigated in further studies whether markers of the fibrinolytic system might be useful for assessment of the prognosis of a coronary intervention in patients with acute coronary syndrome.

Acute Disease↗
PubMed2001

[Atherothrombosis and inflammation].

Alterations of coagulation, fibrinolysis, platelets and low grade inflammation are causal pathophysiological factors in atherosclerosis. Considerable activation of several involved pathways occurs during the acute progression of atherosclerotic lesions, which is characterized by an occluding thrombus, and local and systemic inflammatory reactions as in patients with acute coronary syndromes. These patients become clinically compromised due to the reduction in coronary flow. Furthermore, a frequent occurrence of non-occluding thrombi may be assumed as a progression factor in atherosclerotic diseases. Both the extrinsic and the intrinsic pathway of coagulation are involved, resulting in a hypercoagulative state. Furthermore, an inflammatory acute phase reaction occurs in addition to the activation of several other inflammatory pathways in patients with unstable angina pectoris or acute myocardial infarction. Exposure of tissue factor by the ruptured plaque together with a systemic hypercoagulative state, local and systemic inflammation as well as stimulated platelets and endothelial dysfunction are involved in the pathophysiology of acute coronary syndromes. In the following paper the current knowledge on activation of these pathways and on the various complex interactions is discussed.

Coronary Artery Disease↗
PubMed2001

Acute gender-specific hemodynamic and inotropic effects of 17beta-estradiol on rats.

Estrogen has cardioprotective effects. In addition to beneficial effects on lipid metabolism, estrogen affects the vascular tone and may reduce endothelial dysfunction. In the present study, we examined acute gender-specific hemodynamic and inotropic effects of 17beta-estradiol (17beta-E) versus the control situation in open-chest rats. In addition to measurements in the intact circulation, myocardial function was examined on the basis of isovolumic registration independent of peripheral vascular effects. Regarding the dose-dependent and gender-specific effects of 17beta-E, in female rats, 17beta-E (50, 100, or 200 ng/kg) increased cardiac output (CO) (26%, 43%, and 59% versus control animals) as a result of reduction in total peripheral resistance (TPR) (-13%, -18%, and -24%) without any effect on myocardial contractility (isovolumic left ventricular systolic pressure, -1%, 0%, and -6%). These vascular effects are less pronounced in male rats (for 200 ng/kg 17beta-E: CO, 34%; TPR, -14%). We investigated gender-specific effects of 200 ng/kg 17beta-E after pretreatment with the estrogen receptor (ER) antagonist ICI 182,780. ER blockade reduced the effects of estrogen in female rats (CO, 29%; TPR, -17%) and male rats (CO, 19%; TPR, -11%). Regarding the effects of 200 ng/kg 17beta-E after pretreatment with N(G)-nitro-L-arginine methyl ester, NO synthesis inhibition completely prevented the acute vascular effects of estrogen in female rats (CO, -4%; TPR, 1%). In addition, immunohistochemical staining revealed no gender-specific differences of the vascular ER distribution. 17beta-E caused an acute dose-dependent and gender-specific reduction in the afterload. ERs are involved in both genders in this vasodilative effect that is mediated by NO. This NO-mediated effect may explain in part the cardioprotective effect of estrogen.

Animals↗
PubMed2001

Myocardial troponin T release is associated with enhanced fibrinolysis in patients with acute coronary syndromes.

Patients with acute coronary syndromes (ACS) frequently present with signs of disturbed fibrinolysis. The present study investigates the correlation of alterations in the fibrinolytic system and the amount of myocardial damage characterized by troponin release. In 85 patients with ACS markers of plasmin activation, plasminogen activator system and troponin T (TnT) were measured initially and after 48 h. Patients with TnT release (> or = 0.01 microg/l) at admission had higher TPA levels than those without release (10.2+/-0.7 ng/ml vs. 7.6+/-0.5 ng/ml; p <0.01). Additionally, patients with positive TnT had higher D-dimer levels initially (457+/-39 ng/ml vs. 316+/-22 ng/ml; p <0.01) and 48 h later (451+/-42 ng/ml vs. 275+/-37 ng/ml; p <0.01). The association of myocardial damage with a prothrombotic state and an enhanced fibrinolysis may explain the high prognostic value of troponin measurements in respect to future coronary events.

Acute Disease↗
PubMed2001

[Overview of the relevant aspects of the blood coagulation system--focus and cardiovascular hemostasis].

The hemostasis is a complex regulated system. It can be subdivided into the coagulation cascade, the fibrinolytic system, thrombocytes and cellular hemostasis. In atherosclerosis there are several systemic changes of the hemostasis and fibrinolysis, especially in diabetics. These alterations are markedly pronounced in patients with acute complications like acute coronary syndromes. The alterations in these patients constitute a prothrombotic state. To treat this procoagulant situation several drugs like antithrombins, antiplatelet drugs including glycoprotein IIb/IIIa-receptor antagonists, and others are used. This therapy itself can cause perioperative hemostatic disorders. Therefore, a close communication between cardiologist and cardiac surgeon is necessary to handle this complex situation.

Blood Coagulation↗
PubMed2000

Fibrin specificity and procoagulant effect related to the kallikrein-contact phase system and to plasmin generation with double-bolus reteplase and front-loaded alteplase thrombolysis in acute myocardial infarction.

This study was undertaken to compare the effects of reteplase and alteplase regimens on hemostasis and fibrinolysis in acute myocardial infarction (AMI). Thrombolytic treatment in patients with AMI is hampered by paradoxical procoagulant effects that favor early reocclusion. In vivo data comparing this effect and the fibrin specificity of double-bolus reteplase and front-loaded alteplase regimens are not available. In a prospective, randomized study, 50 patients with AMI were either treated with double bolus (10 + 10 U) reteplase or with front-loaded alteplase (up to 100 mg) within 6 hours of symptom onset. Thirty apparently healthy persons served as controls. Molecular markers of coagulation and fibrinolysis were serially examined for up to 5 days. Paradoxical thrombin activation at 3 hours after initiation of therapy was comparable between reteplase and alteplase. Reteplase (65 +/- 5 U/L) and alteplase (72 +/- 8 U/L) caused significantly elevated kallikrein activity at 3 hours after adminstration (p <0.01 vs controls 30 +/- 1 U/L). Fibrin specificity was less for reteplase (p <0.05) with a decrease in fibrinogen at 3 hours to 122 +/- 27 mg/dl versus 224 +/- 28 mg/dl for alteplase (p <0.01 and p <0.05 vs controls). D-Dimer levels at 3 hours were higher (p <0.05) after reteplase (5,459 +/- 611 ng/ml) versus alteplase (3,445 +/- 679 ng/ml) (both p <0.01 vs controls 243 +/- 17 ng/ml). Plasmin generation (plasmin-antiplasmin complexes) was significantly (p <0.01) increased at 3 hours with both regimens to 27,079 +/- 3,964 microg/L (reteplase) and 19,522 +/- 2,381 microg/L (alteplase). The data from 3 hours after start of thrombolytic therapy proved less marked fibrin specificity of the reteplase regimen (in vivo) compared with front-loaded alteplase. Both regimens have a moderate procoagulant effect without differences in activation of the kallikrein system.

Adult↗
PubMed2000

[A standardized documentation structure for data documentation in echocardiography. Work Team on Standards and LV Function of the Work Group on Cardiovascular Ultrasound of the German Society of Cardiology, Heart and Circulation Research].

Presently, there are no well-defined standards for documentation of echocardiographic studies. Nevertheless, standards are essential to provide comparability of data and to realize electronic communication, both essential for quality management in echocardiography. Therefore, the working group "Standards and LV function" of the German Society of Cardiology developed a consensus for documentation of echocardiographic studies. In the present paper this consensus is presented and illustrated by typical clinical examples. Additionally, a prototype of a user-oriented software based on this data set is presented. The complete data set for transesophageal and transthoracic echocardiography and the software prototype can be downloaded at http:@echo.ma.uni-heidelberg.de.

Aortic Valve Stenosis↗
PubMed1999

[Blood coagulation and fibrinolysis in arteriosclerosis].

Thrombus formation at the site of atherosclerotic lesions, especially on a ruptured plaque, plays a central role in the "atherothrombosis" hypothesis. An activation of the hemostasis and a disturbed fibrinolysis are known. These alterations are especially marked in patients with acute coronary syndromes. In stable coronary artery disease, fibrinogen is elevated. Furthermore, minor alterations of the contact phase factor VII and consecutively of the thrombin system are detectable depending on the study population. Thrombin generation and activation become marked in patients with unstable angina pectoris or acute myocardial infarction. Possible reasons for this activation are an activation of the contact phase factor XII system and the release of tissue factor both from the ruptured plaque and from stimulated monocytes. The fibrinolytic system is markedly altered already in patients with stable coronary heart disease. Increased levels of tissue-type plasminogen activator and of urokinase-type plasminogen activator/receptor are measurable in atheromas. Tissue-type plasminogen activator mass concentration is systemically elevated already at early stages of atherosclerosis. Especially in patients with increased risk for acute coronary syndromes, the plasminogen activator inhibitor activity is significantly increased. Furthermore, a hypercoagulative state with increased d-dimer levels and plasmin-antiplasmin complexes can be measured. The alterations of hemostasis and especially of fibrinolysis are detectable for prolonged time period and persist much longer than the clinical symptoms of the patients. The increased plasminogen activator inhibitor activity is associated with the metabolic syndrome and constitutes an (in part genetically determined) disturbance in patients with stable or unstable coronary heart disease. However, the large intra- und interobserver as well as diurnal variability of this marker limits its use as a routine measure for risk stratification in patients. Alterations of the hemostasis and disturbances of fibrinolysis are detectable during the chronic as well as the acute phase of atherosclerosis. These changes are best documented for coronary heart disease, whereas less data are available for other manifestations of atherosclerosis. The use of newly developed molecular markers for single reaction steps of pathways instead of global functional tests and of new molecular biological methods did considerably improve the detailed knowledge on the pathomechanisms of the development of atherosclerosis, making the development of targeted therapies, e.g., against receptors possible. Future studies will investigate the quantitative impact of the various activated pathways (cause or reaction) and the effects of interventions on these pathomechanisms in patients with acute coronary syndromes. Studies will have to focus especially on the meaning of polymorphisms, early changes in the development of atherosclerosis and interactions with inflammatory processes.

Blood Coagulation Factors↗