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Biomedical subjects

Bodo E Strauer

Publications and source records attributed to Bodo E Strauer.

At least 19 recordsLinked to original sources
PubMed2006

[Hypertension and heart].

The term hypertensive heart disease covers the entities left ventricular hypertrophy, microangiopathy, diastolic and systolic dysfunction, und increased risk of arrhythmias. From the pathophysiological point of view this is caused by hypertrophy of cardiac myocytes, interstitial fibrosis and media hypertrophy of the arterioles. As an earliest sign of hypertensive heart disease a microangiopathy can be diagnosed. Also a diastolic dysfunction can be found as an early change. In further persisting arterial hypertension left ventricular hypertrophy develops (often asymmetric), and later a systolic dysfunction. Clinically, the patients suffer from angina pectoris, dyspnea and rhythm disorders. Left ventricular hypertrophy is associated with an increased risk of ventricular malignant arrhythmias. Thus, the main therapeutic principle should be antihypertensive therapy with the goal of regression of hypertrophy and, as a consequence, a decreased mortality risk.

Arrhythmias, Cardiac↗
PubMed2006

[Chemoreflexsensitivity is reduced in obstructive sleep apnea and might be modulated by the autonomic system].

BACKGROUND: Chemoreflexes are important mechanisms for regulating ventilatory and cardiovascular function, which are supposed to be influenced in obstructive sleep apnea (OSA). PATIENTS AND METHODS: For determination of chemoreflexsensitivity (CHRS) the ratio of the RR-interval shift in the surface ECG during 5 min inhalation of oxygen via a nose mask was formed in 15 patients with suspected OSA. Noradrenaline plasma concentrations were measured and were correlated to CHRS. RESULTS: Patients with OSA showed a reduced CHRS. CHRS was correlated to the severity of sleep apnea (respiratory disturbance index [RDI]; r = -0.622; p = 0.013), and to minimal nocturnal oxygen saturation (r = 0.594; p = 0.032). Reduced CHRS was associated with higher noradrenaline concentrations (r = -0.542; p = 0.037). CONCLUSION: CHRS is reduced in patients with OSA and correlates with the severity of OSA. Further on, CHRS might be modulated by the autonomic system. Therefore, the determination of CHRS enables to estimate sympathetic activation in these patients.

Adult↗
PubMed2006

Stem cell therapy in postinfarction chronic coronary heart disease.

After acute myocardial infarction, bone-marrow-derived cells (BMDCs) improve cardiac function; it is conceivable, but not yet demonstrated, that BMDC therapy might also be useful in chronic infarction. We treated 18 consecutive patients who had chronic myocardial infarction (between 5 months and 8.5 years postinfarction) using intracoronary transplantation of autologous BMDCs and compared this group with a representative control group who did not receive cell therapy. After 3 months, infarct size in the transplantation group was reduced by 30% and both global left ventricular ejection fraction and infarction wall-movement velocity were increased significantly (15% and 57%, respectively), whereas in the control group no significant changes were observed. After transplantation of BMDCs, there was an 11% improvement in maximum oxygen uptake and a 15% increase in regional (18)F-fluordeoxyglucose uptake into infarcted tissue, as determined by positron emission tomography. These results show that functional and metabolic regeneration of infarcted and chronically avital tissue can be achieved in humans using transplantation of bone-marrow-derived cells.

Bone Marrow Cells↗
PubMed2005

Regeneration of human infarcted heart muscle by intracoronary autologous bone marrow cell transplantation in chronic coronary artery disease: the IACT Study.

OBJECTIVES: Stem cell therapy may be useful in chronic myocardial infarction (MI); this is conceivable, but not yet demonstrated in humans. BACKGROUND: After acute MI, bone marrow-derived cells improve cardiac function. METHODS: We treated 18 consecutive patients with chronic MI (5 months to 8.5 years old) by the intracoronary transplantation of autologous bone marrow mononuclear cells and compared them with a representative control group without cell therapy. RESULTS: After three months, in the transplantation group, infarct size was reduced by 30% and global left ventricular ejection fraction (+15%) and infarction wall movement velocity (+57%) increased significantly, whereas in the control group no significant changes were observed in infarct size, left ventricular ejection fraction, or wall movement velocity of infarcted area. Percutaneous transluminal coronary angioplasty alone had no effect on left ventricular function. After bone marrow cell transplantation, there was an improvement of maximum oxygen uptake (VO2max, +11%) and of regional 18F-fluor-desoxy-glucose uptake into infarct tissue (+15%). CONCLUSIONS: These results demonstrate that functional and metabolic regeneration of infarcted and chronically avital tissue can be realized in humans by bone marrow mononuclear cell transplantation.

Adult↗
PubMed2005

Altered blood rheology in obstructive sleep apnea as a mediator of cardiovascular risk.

BACKGROUND: Cardiovascular complications are common in patients with obstructive sleep apnea (OSA). Blood rheology is a major determent of coagulation and an established risk factor for cardiovascular events. Since nocturnal hypoxemia could influence parameters of blood rheology, we hypothesized that OSA alters blood rheology independent of other cardiovascular risk factors. METHODS: One hundred and ten consecutive patients admitted to the sleep laboratory were included. The association of plasma fibrinogen and viscosity (as parameters of blood rheology) with OSA was evaluated. RESULTS: One hundred and ten patients aged 61.4+/-10.1 years (body mass index 28.4+/-4.1 kg/m2) were included. OSA was confirmed in 63 patients (57.2%) with an apnea-hypopnea index (AHI) of 28.7+/-14.9 events/hour. Patients with OSA showed higher levels of plasma viscosity (1.36+/-0.09 vs. 1.31+/-0.08 mPas, p=0.005). Nevertheless, hypertensive apneics have even higher levels of plasma viscosity than nonapneics (1.38+/-0.091 vs. 1.32+/-0.028 mPas, p=0.018). Similar results were found in patients with coronary artery disease, where OSA was associated with elevated plasma viscosity (1.36+/-0.076 vs. 1.31+/-0.081 mPas, p=0.007). Plasma fibrinogen was correlated with nocturnal minimal oxygen saturation (r=-0275, p=0.0036) and AHI (r=0.297, p=0.001). OSA was associated with higher plasma fibrinogen (353+/-83 vs. 317+/-62 mg/dl, p=0.015). These differences persist with control for cardiovascular risk factors. CONCLUSIONS: Patients with OSA have elevated morning fibrinogen levels and a higher plasma viscosity, which correlate positively with indices of sleep apnea severity. These changes in blood rheology are independent of cardiovascular risk factors, and therefore, might be specific mechanisms of OSA. This supports the pathophysiological concept that sleep apnea is a cardiovascular risk factor.

Adult↗
PubMed2005

Reduction of peripheral flow reserve impairs endothelial function in conduit arteries of patients with essential hypertension.

BACKGROUND: A diminished flow reserve in resistance vessels is a hallmark of hypertensive microvascular disease. Hypertension is associated with structural alterations in the microcirculation and a reduced endothelium-dependent dilation in conduit arteries. Both have been demonstrated to predict future cardiovascular events. OBJECTIVE: We hypothesized that a reduced peripheral flow reserve impairs endothelial function in upstream conduit arteries in patients with arterial hypertension. DESIGN: In 43 hypertensive patients (HT) and 38 normotensive controls (NT) endothelial function of the brachial artery was assessed by measurement of flow-mediated dilatation (FMD), using high-resolution ultrasound. Peripheral flow reserve (FR) was determined via measurements of forearm blood flow at rest and during increments of reactive hyperaemia, using venous occlusion plethysmography. RESULTS: FMD was markedly impaired in HT (3.6 +/- 0.3%) as compared with NT (10.2 +/- 0.3%), whereas maximum brachial artery diameter following endothelium-independent dilatation was similar in both groups. In hypertensive patients FR was significantly reduced (HT, 3.2 versus NT, 6.0) during reactive hyperaemia after 5 min of ischaemia. FR was associated with FMD (r = 0.68, P < 0.01). Multiple stepwise regression analysis identified FR as a strong independent variable determining the extent of FMD (r2 = 0.46, P < 0.01). In HT the dose-response curve of FMD upon stepwise increases of FR was shifted significantly to the right. Normalization of FR improved FMD in HT by more than 60%. CONCLUSIONS: In essential hypertension a reduced FR contributes to the endothelial dysfunction of upstream conduit arteries. These findings may have therapeutic and prognostic implications in patients with arterial hypertension.

Adult↗
PubMed2004

Coronary flow reserve measurements in hypertension.

Taken together, the diagnostic algorithm is leaded by a simple ECG stress test. In case of ST-segment depression the preferred image test should be stress ECG to bring patients at high risk for significant epicardial coronary artery stenosis to coronary angiography (and revascularization). In case of the lack of wall motion abnormalities (during stress-echo test) or absence of epicardial stenosis one may further assess coronary flow reserve with noninvasive Doppler harmonic echocardiography. For ultimate quantitative assessment invasive procedures, such as argon dilution or intracoronary Doppler techniques, represent the appropriate approach. Treatment of microvascular disease may be followed-up by these new noninvasive diagnostic approaches in future and also, at present, by monitoring ST-segment depression.

Angiography↗
PubMed2003

[Stem cell therapy in acute myocardial infarction].

Remodeling of the left ventricle after myocardial infarction represents a major cause of infarct-related heart failure and death. Experimental data suggest that bone marrow-derived cells may contribute to the healing of myocardial infarction. The selective intracoronary transplantation of autologous, mononuclear bone marrow cells is safe and seems to be effective under clinical conditions concerning heart function, myocardial perfusion, and metabolism. The therapeutic effect may be attributed to bone marrow cell-associated myocardial regeneration and neovascularization.

Angioplasty, Balloon, Coronary↗
PubMed2003

[Regression of left ventricular hypertrophy in hypertensive heart disease].

PATHOPHYSIOLOGY AND THERAPY: Left ventricular hypertrophy represents an important factor determining the prognosis of hypertensive patients. Hypertrophy as identified by electrocardiography (Table 1) or echocardiography (Table 2) characterizes patients with a significantly increased risk of mortality and arrhythmia. From the pathophysiological point of view this is based on hypertrophy of the media in resistance vessels, on interstitial fibrosis, on a reduced coronary flow reserve and on the occurrence of ischemia (Figure 1). The diastolic and (later) systolic function of the heart are disturbed (Figures 2 to 4). Antihypertensive therapy with beta blockers and diuretics leads to a reduction of left ventricular mass by 5-8%, with ACE-inhibitors and AT-blockers by 13% (Figure 5). Particularly ACE-inhibitors can effectively reverse of the above mentioned pathological processes. Regression of hypertrophy goes along with an improved prognosis and a reduction of atrial and ventricular arrhythmias (Figure 6). A symptomatic treatment of arrhythmias should always be accompanied by medical therapy aimed at regression of hypertrophy. Optimal therapy results in normalizes of blood pressure, leads to a regression of hypertrophy and induces cardiac reparation, which in turn improve left ventricular function, reduces microvascular ischemia stress and arrhythmias. These therapeutic desiderates are also pertinent for hypertensive heart disease in the prehypertrophic state, as in juvenile hypertension.

Adrenergic beta-Antagonists↗
PubMed2003

Direct biochemical evidence for eNOS stimulation by bradykinin in the human forearm vasculature.

OBJECTIVE: Although it has been shown recently that acetylcholine (ACh)-induced vasodilation of forearm resistance vessels is predominantly mediated by nitric oxide, direct biochemical evidence for eNOS stimulation by bradykinin (BK) in the human arterial circulation is still lacking. Therefore, the present study was designed to test the hypothesis that in the human forearm vasculature eNOS stimulation significantly contributes to BK-induced vasodilation. METHODS: BK was infused in the presence and absence of the NOS inhibitor L-NMMA (8 micromol/min) into the brachial artery of 16 healthy volunteers and the effects compared to muscarinergic eNOS stimulation following acetylcholine infusion. Forearm blood flow (FBF) was measured by venous occlusion plethysmography, and plasma nitrite (NO(2)(-)), which represents a sensitive and specific marker of regional eNOS activity, was determined in the antecubital vein and brachial artery by flow injection analysis. Nitric oxide production was calculated as product of the veno-arterial difference of NO(2)(-) concentration times FBF. RESULTS: Kininergic (BK: 20, 60, 200 ng/min) as well as muscarinergic (ACh: 1, 3, 10 microg/min) stimulation resulted in a dose-dependent increase in FBF and NO(2)(-) in each individual. The relationship between FBF and NO production upon BK infusion was comparable to that obtained with ACh (r = 0.98; n = 64, p < 0.01). Moreover, NOS inhibition reduced both flow responses and NO production (BK: 54 and 75 %; ACh: 57 and 72 %) to a similar extent. CONCLUSIONS: These data provide direct biochemical evidence for the involvement of eNOS in bradykinin-induced vasodilation of forearm resistance vessels in humans.

Acetylcholine↗
PubMed2003

Long-term follow-up of sudden cardiac arrest survivors and electrophysiologically guided antiarrhythmic therapy.

Sudden cardiac arrest survivors have a high risk of suffering from recurrent arrhythmic events. Recent studies have shown that these patients have a significantly decreased mortality rate, if they are supplied with an implantable cardioverter/defibrillator (ICD). The aim of this study was to evaluate the long-term prognosis of patients with electrophysiologically guided antiarrhythmic drug therapy in comparison to patients with ICD. 204 consecutive survivors of sudden cardiac arrest were enrolled in this study. All patients were examined with an initial electrophysiologic study (EPS) with programmed ventricular stimulation. Patients were treated with antiarrhythmic drugs (if the inducible tachycardia was suppressed) or with the implantation of an ICD. The maximal follow-up period was 120 months, the mean period was 53.3 +/- 31.4 months (ICD) versus 60.3 +/- 35.5 months (EPS, nonsignificant). Patients with ICD showed an overall mortality rate of 14.6%, whereas EPS-guided patients had a mortality rate of 43.2% (p < 0.001). The cardiac and arrhythmogenic mortality rates were significantly lower in the ICD group (12 vs. 43%, p < 0.01, and 1 vs. 16%, p < 0.001, respectively). A reduction of the mortality risk was observed in the ICD group by up to 61% (all-cause mortality), 52% (cardiac mortality) and 97.2% (arrhythmogenic mortality). In arrhythmic event survivors with ICD, arrhythmic and overall mortality rates are significantly lower compared to patients with an EPS-guided drug therapy. In the secondary prevention of sudden cardiac death, ICD should be the first choice of antiarrhythmic therapy.

Adult↗
PubMed2003

Enlarged effects of adenosine in a septic patient with multiple myeloma and atrial flutter.

We report the history of a 60-year-old patient with a multiple myeloma and Staphylococcus aureus associated sepsis to whom adenosine in a dose of 6 mg was administered, when a regular, narrow QRS complex tachycardia at a heart rate of 120 beats/minute started. Adenosine led to a complete AV-block and revealed atrial flutter. Atrial flutter waves persisted for about 15 seconds and were followed by atrial and ventricular asystole for about 20 seconds. Repeated nonsustained polymorphic ventricular tachycardias followed and after about 90 seconds sinus rhythm was restored.

Adenosine↗
PubMed2003

Parameters of left ventricular diastolic function 48 hours after coronary angioplasty and stent implantation.

INTRODUCTION: It has been reported that stent implantation results in an earlier and more pronounced improvement of coronary flow reserve in comparison to conventional balloon angioplasty. Whether this phenomenon translates into hemodynamic changes of left ventricular systolic and diastolic function has not been investigated. This study was designed to determine whether stenting leads to greater changes in measures of diastolic dysfunction than plain angioplasty alone. METHODS: Parameters of diastolic function were ascertained by Doppler echocardiography in 194 patients with single-vessel disease before and 48 hours after elective coronary angioplasty. A total of 116 patients were initially successfully treated with coronary angioplasty. In 78 patients, stents were used to improve an inadequate result after coronary angioplasty. The parameters of left ventricular diastolic function were evaluated before and 48 hours after coronary intervention by Doppler echocardiography. Ejection fraction was determined and used to characterize systolic left ventricular function. RESULTS: Both patient groups (116 patients with coronary angioplasty, 78 patients with combined coronary angioplasty and stent implantation) showed no relevant differences concerning sex, age, atherosclerotic risk factors, exercise capacity and results of exercise electrocardiography. All patients who underwent stent implantation showed an early improvement of left ventricular diastolic function 48 hours after intervention. Surprisingly, there was no significant short-term improvement (48 hours) of diastolic function in patients with initially successful angioplasty. CONCLUSION: Stent implantation results in improved left ventricular diastolic function in comparison to conventional balloon angioplasty. This has to be attributed to a more immediate and increased antiischemic effectiveness due to the scaffolding properties of stents.

Aged↗
PubMed2002

Repair of infarcted myocardium by autologous intracoronary mononuclear bone marrow cell transplantation in humans.

BACKGROUND: Experimental data suggest that bone marrow-derived cells may contribute to the healing of myocardial infarction (MI). For this reason, we analyzed 10 patients who were treated by intracoronary transplantation of autologous, mononuclear bone marrow cells (BMCs) in addition to standard therapy after MI. METHODS AND RESULTS: After standard therapy for acute MI, 10 patients were transplanted with autologous mononuclear BMCs via a balloon catheter placed into the infarct-related artery during balloon dilatation (percutaneous transluminal coronary angioplasty). Another 10 patients with acute MI were treated by standard therapy alone. After 3 months of follow-up, the infarct region (determined by left ventriculography) had decreased significantly within the cell therapy group (from 30+/-13 to 12+/-7%, P=0.005) and was also significantly smaller compared with the standard therapy group (P=0.04). Likewise, infarction wall movement velocity increased significantly only in the cell therapy group (from 2.0+/-1.1 to 4.0+/-2.6 cm/s, P=0.028). Further cardiac examinations (dobutamine stress echocardiography, radionuclide ventriculography, and catheterization of the right heart) were performed for the cell therapy group and showed significant improvement in stroke volume index, left ventricular end-systolic volume and contractility (ratio of systolic pressure and end-systolic volume), and myocardial perfusion of the infarct region. CONCLUSIONS: These results demonstrate for the first time that selective intracoronary transplantation of autologous, mononuclear BMCs is safe and seems to be effective under clinical conditions. The marked therapeutic effect may be attributed to BMC-associated myocardial regeneration and neovascularization.

Angioplasty, Balloon, Coronary↗
PubMed2002

Incidence and clinical outcome of iatrogenic femoral arteriovenous fistulas: implications for risk stratification and treatment.

OBJECTIVES: We sought to determine the incidence of arteriovenous fistulas (AVF), identify risk factors for AVF, and follow up the clinical outcome of femoral AVF. BACKGROUND: Arteriovenous fistulas are a potential harmful complication of cardiac catheterization. Incidence and clinical outcome of iatrogenic AVF are unknown so far, although important for risk stratification and treatment. METHODS: A total of 10,271 consecutive patients undergoing cardiac catheterization were followed up prospectively over a period of three years. Diagnosis of AVF was performed by duplex sonography. RESULTS: The incidence of AVF was 0.86% (n = 88). The following significant and independent risk factors for AVF were identified: high heparin dosage (odds ratio [OR]) = 2.88), coumadin therapy (OR = 2.34), puncture of the left groin (OR = 2.21), arterial hypertension (OR = 1.86), and female gender (OR = 1.84). Within 12 months 38% of all AVF closed spontaneously. No signs of cardiac volume overload or limb damage were observed in patients with persisting AVF. None of the risk factors for AVF influenced the incidence or the rate of AVF closure. Only intensified anticoagulation showed a tendency to extend AVF persistence. CONCLUSIONS: Almost 1% of patients undergoing cardiac catheterization acquire femoral AVF, for which patient- and procedure-related risk factors could be identified. One-third of iatrogenic AVF close spontaneously within one year. Cardiac volume overload and limb damage are highly unlikely with AVF persistence. Thus, a conservative management for at least one year seems to be justified.

Aged↗