[Hypertension and heart]. / Hochdruck und Herz.

Arterial hypertension often leads to diseases of kidneys, vessels and brain. Besides these end organ damages the changes of the heart are of important role. Substantial consequences of hypertension are microangiopathy, interstitial fibrosis and left ventricular hypertrophy. Hence, as an early stage diastolic dysfunction results. Due to longer persistent hypertension also systolic dysfunction develops. Clinically, patients suffer from angina pectoris, dyspnoea and cardiac arrhythmias (i.e. atrial arrhythmia, atrial fibrillation). The left ventricular hypertrophy also is associated with an increased risk of malignant ventricular arrhythmias. The risk of sudden cardiac death is raised as well, in particular in patients with dilated heart and reduced left ventricular ejection fraction. Well controlled antihypertensive therapy could lead to a regression of left ventricular hypertrophy. Hence, disorders and prognosis of the patients could be improved.

Therapeutic potentials of stem cells in cardiac diseases.

Coronary heart disease and chronic heart failure are common diseases and have an increasing frequency. Although interventional and conventional drug therapy may delay ventricular remodelling, there is no basic therapeutic regime available for preventing or even reversing this process. Chronic coronary artery disease and heart failure impair quality of life and are associated with subsequent worsening of the cardiac pump function. Numerous studies carried out in the past few years have demonstrated, that the intracoronary stem cell therapy has to be considered as a safe therapeutic procedure in heart disease, when destroyed and/or compromised heart muscle must be regenerated. This kind of cell therapy with autologous bone marrow cells is completely justified ethically, except for the small numbers of patients with direct or indirect bone marrow disease (e.g. myeloma, leukemic infiltration) in whom there would be lesions of mononuclear cells. Several preclinical as well as clinical trials have shown that transplantation of autologous bone marrow cells or precursor cells improved cardiac function after myocardial infarction and in chronic coronary heart disease. The age of infarction seems to be irrelevant to regenerative potency of stem cells, since stem cells therapy in old infarctions (many years old) is almost equally effective in comparison to previous infarcts. Further indications are non-ischemic cardiomyopathy (dilatative cardiomyopathy) and heart failure due to hypertensive heart disease.

[Stem cell therapy for cardiovascular diseases. Experiences in Düsseldorf]. / Stammzelltherapie bei kardiovaskulären Erkrankungen. Düsseldorfer Erfahrungen.

The selective transplantation of autologous bone marrow cells (chronic infarction 10 (9) million cells) as well as the intracoronary approach, represents a novel and effective therapeutic procedure. The improvement of autologous stern cell therapy is achieved in addition to the catheter interventional procedures and is a procedure for regeneration of destroyed heart muscle in the early phase after myocardial infarction. In patients with chronic coronary artery disease (mean 108 months after myocardial infarction) intracoronary stern cell therapy leads to significant increase of left ventricular pump function and contractility, reduction of infarct size, increase of myocardial glucose storage and an increase of physical ability (functional capacity) and feeling of well-being. Autologous stern cell therapy in patients with dilated cardiomyopathe seems to be a new option for myocardial restitution. A significant improvement of the subjective aas well as the objective functional capacity was documented. Also a significant reduction of ventricular arrhythmias was revealed in patients with chronic coronary artery disease and non-ischemic cardiomyopathy. Stern cells have the important properties of self-regeneration and organ plasticity. Therefore they are ideal candidates for regeneration of myocardial tissue. The regenerative potential of bone-marrow-derived stern cells may be explained by four mechanisms: 1) direct cell differentiation from monoclear cells to cardiac myocytes, 2) cytokine-induced growing and increase of residual viable myocytes, especially within the border zone of the infracted area, 3) stimulation of resident cardiac stern cells (endogenous stern cells), and 4) induction of cell fusion between transplanted bone marrow cells and resident myocytes. For this method of therapy, no ethical problems exist, and no side effects were observed. The therapeutic benefit for the patient's heart seems to prevail. Peripheral arterial occlusion disease The combined intraarterial and intramuscular transplantation of autologous, mononuclear bone marrow stern cells is a clinical feasible and safe therapeutical option for patients with severe chronic limb ischemia. It leads to a significant increase of the perfusion indices and of the quality of life. Further studies are required to prove the benefit of these new therapeutic approach.

The therapeutic potential of stem cells in heart disease.

Coronary heart disease and chronic heart failure are common and have an increasing frequency. Although interventional and conventional drug therapy may delay ventricular remodelling, there is no basic therapeutic regime available for preventing or even reversing this process. Chronic coronary artery disease and heart failure impairs quality of life and are associated with subsequent worsening of the cardiac pump function. Numerous studies within the past few years have been demonstrated, that the intracoronary stem cell therapy has to be considered as a safe therapeutic procedure in heart disease, when destroyed and/or compromised heart muscle must be regenerated. This kind of cell therapy with autologous bone marrow cells is completely justified ethically, except for the small numbers of patients with direct or indirect bone marrow disease (e.g. myeloma, leukaemic infiltration) in whom there would be lesions of mononuclear cells. Several preclinical as well as clinical trials have shown that transplantation of autologous bone marrow cells or precursor cells improved cardiac function after myocardial infarction and in chronic coronary heart disease. The age of infarction seems to be irrelevant to regenerative potency of stem cells, since stem cells therapy in old infarctions (many years old) is almost equally effective in comparison to previous infarcts. Further indications are non-ischemic cardiomyopathy (dilative cardiomyopathy) and heart failure due to hypertensive heart disease.

Factors influencing spontaneous mobilization of CD34+ and CD133+ progenitor cells after myocardial infarction.

BACKGROUND: Bone marrow-derived circulating progenitor cells (BM-CPCs) are mobilized into adult peripheral blood (PB) during acute myocardial infarction (AMI) and may contribute to the regeneration of infarcted myocardium. The purpose of the present study is to determine whether mobilization of BM-CPCs into PB depends on cardiovascular risk factors (CVRFs), age of patients, infarct associated inflammatory markers, and left ventricular function after AMI. MATERIALS AND METHODS: Peripheral blood concentrations of CD34/45(+) and CD133/45(+) BM-CPCs were measured by flow cytometry in 44 patients after AMI and in 16 subjects with atypical chest pain acting as controls. RESULTS: Mobilization of CD34/45(+) and CD133/45(+) BM-CPCs on day 1 after AMI showed significant negative correlation with age, the number of CVRFs, infarct size, creatine phosphokinase peak in bivariate as well as in multivariate analyses. We additionally found a positive correlation of CD34/45(+) and CD133/45(+) BM-CPCs mobilization on day 1 after AMI with global ejection fraction (EF) in bivariate analysis but could not confirm this in multivariate analysis. Elevated of C-reactive protein (CRP) and leukocyte levels on day 1 after AMI were significantly associated with decreased concentrations of CD34/45(+) BM-CPCs. The concentrations of CD34/45(+) and CD133/45(+) BM-CPCs significantly increased in AMI patients, with the peak on day 7 as compared to the control group. CONCLUSIONS: The mobilization of CD34/45(+) and CD133/45(+) BM-CPCs into the PB depends on many factors, i.e. the number of CVRFs, age, infarct size and inflammatory markers of patients. Most importantly, the severity of the circulatory dysfunction and the amount of necrotic myocardial tissue are the main determinants. Moreover, this spontaneous mobilization of BM-CPCs may serve as a very important surrogate for infarct size as well as for global EF and it may determine the regenerative potency after AMI.

[Hypertension and cardiac failure]. / Hochdruck und Herzinsuffizienz.

Arterial hypertension is the leading cause of mortality and morbidity with a worldwide prevalence of 26%. Aging increases the incidence of arterial hypertension. Arterial hypertension is the prime example for a chronic disease with asymptomatic beginning, creeping course and fatal outcome. Arterial hypertension is a major cardiovascular risk factor and leads to vascular as well as myocardial manifestations: coronary artery disease, hypertensive microvascular disease, concentric left ventricular hypertrophy as well as perivascular and interstitial fibrosis. In the late stages of the disease, hypertrophy and cardiac failure develop. Arterial hypertension is the leading cause of coronary artery disease and cardiac failure, and coronary artery disease is the cause of heart failure in 50% of cases. Various non-invasive and invasive procedures are available for screening and follow-up. The primary therapeutic target is to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms as well as lowering blood pressure. This article covers the pathophysiology of arterial hypertension and cardiac failure, clinical symptoms, diagnostic options and therapeutical goals as well as medicinal options.

Diagnostics in pulmonary hypertension.

Pulmonary hypertension is a serious disease with a poor prognosis. Pulmonary hypertension is defined by a mean pulmonary arterial pressure over 25 mm Hg at rest or over 30 mm Hg during activity. According to the recent WHO classification from 2003 pulmonary hypertension can be categorized as pulmonary arterial hypertension, pulmonary venous hypertension, hypoxic pulmonary hypertension, chronic thromboembolic pulmonary hypertension and pulmonary hypertension from other causes. Pulmonary arterial hypertension is characterized histopathologically by vasoconstriction, vascular proliferation, in situ thrombosis, and remodeling of all 3 levels of the vascular walls. These pathologic changes result in progressive increases in the mean pulmonary artery pressure and pulmonary vascular resistance, which, if untreated leads to right-ventricular failure and death. Early in the disease process, the signs and symptoms of PAH are often nonspecific, making diagnosis challenging. Patients often present with progressively worsening dyspnea and fatigue. Patients with severe pulmonary arterial hypertension die of right heart failure. The diagnostic procedures include clinical history and physical examination, a standard chest radiography, electrocardiography, transthoracic Doppler echocardiography, pulmonary function tests, arterial blood gas analysis, ventilation and perfusion lung scan, high-resolution computed tomography of the lungs, contrast-enhanced spiral computed tomography of the lungs and pulmonary angiography, blood tests and immunology, abdominal ultrasound scan, exercise capacity assessment, and hemodynamic evaluation. Invasive and non-invasive markers of disease severity, either biomarkers or physiological parameter and tests that can be widely applied, have been proposed to reliably monitor the clinical course. Pulmonary biopsy is rarely indicated. Transthoracic echocardiography is a key screening tool in the diagnostic algorithm. Because transthoracic echocardiography is an inexpensive, easy, and reproducible method, it is the most commonly used noninvasive diagnostic tool to determine pulmonary arterial pressure. But it not only provides an estimate of pulmonary pressure at rest and during exercise, but it may also help to exclude any secondary causes of pulmonary hypertension, predict the prognosis, monitor the efficacy of specific therapeutic interventions, and detect the preclinical stage of the disease. In addition, the measurement of serum markers, such as brain natriuretic peptide (BNP), are diagnostically useful and of prognostic significance. Once the diagnosis and etiology of pulmonary hypertension have been established, several parameters can predict outcome in these patients: functional class, right ventricular function, pulmonary hemodynamics, and certain laboratory parameters. Also, exercise parameters such as walking distance, peak oxygen uptake or peak systolic blood pressure can reliable predict prognosis in these patients.

Signal-averaged P-wave ECG as a marker of atrial electrical instability in patients with right ventricular dysfunction.

Severe pulmonary hypertension (PAH) leads to right ventricular dysfunction and is associated with different atrial arrhythmias. In PAH patients, the echocardiographic Tei-index is used for monitoring right heart function. The P-wave signal-averaged ECG (SA-ECG) has been shown to have a potential role in identifying patients at risk of developing paroxysmal atrial fibrillation and those likely to change from paroxysmal to chronic atrial fibrillation. The aim of the present study was to define the correlation of the Tei-Index with parameters of P-wave triggered and bidirectional P-wave SA-ECG. A total of 18 patients (14 men, 4 women) with normal sinus rhythm and a mean age of 67+/-10 years (BMI 27.6+/-5.1 kg/m2) were included into the study. Right ventricular (RV) Tei-index was calculated from the sum of isovolumetric contraction time and relaxation time divided by ejection time. Furthermore, P-wave triggered P-wave signal averaged ECG was performed from an X, Y, and Z lead system. The results show that there was a statistically significant correlation between Tei-index and filtered P-wave duration (r=0.53; P=0.023). Teiindex did not correlate with the root mean square voltage of the last 20 ms of the P wave (r=-0.16; P=0.52). In conclusion, a correlation of RV Tei index with P-wave duration indicates that this echocardiographic measurement is not only a marker of right heart function, but also an indicator of electrical instability that could be useful to detect patients at risk for atrial arrhythmias.

Effects of continuous positive airway pressure on exercise capacity in chronic heart failure patients without sleep apnea.

Continuous positive airway pressure (CPAP) is an effective treatment for obstructive sleep apnea. It is known, that there are beneficial effects on cardiac function, which might be explained by suppression of apnea and specific hemodynamic effects of CPAP. Therefore, CPAP might act as an adjunct therapy in heart failure, even in the absence of sleep apnea. In the present study, 11 patients with congestive heart failure (EF=23.1+/-6.9%) without sleep apnea (AHI 3.0+/-1.2/h) were treated with nocturnal CPAP. Cardiopulmonary exercise testing was performed at baseline and after 8.6 +/-1.3 months. All patients underwent heart catheterization and myocardial biopsy to exclude myocarditis at baseline. Five (46%) of the 11 patients did not complete the study because of poor compliance and irregular use of the CPAP device. Six (54%) of the patients used CPAP regularly (>6 h/night) and completed the study. Cardiopulmonary exercise testing showed an improvement of work load (96+/-36 Watt vs. 112+/-34 Watt; P=0.025) and VO2 peak (1227+/-443 ml vs. 1525+/-470 ml; P=0.01). Oxygen-pulse was increased, although that did not reach significance (11.2+/-4.8 ml/beat vs. 12.6+/-3.9 ml/beat). In conclusion, CPAP might have beneficial effects on exercise capacity in patients with congestive heart failure even in the absence of sleep apnea. Nevertheless, poor compliance seems to be a limiting factor.

[CPAP as adjunctive treatment option for chronic heart failure]. / CPAP-Therapie als additive/adjuvante Herzinsuffizienztherapie?

Chronic heart failure with its age-dependent prevalence and incidence is one of the most frequent diseases. Due to high mortality and morbidity there is the necessity of early diagnosis and therapeutic measures being as causal as possible. The medical graded therapy is based on the combination of ACE-inhibitors/AT1-blockers, beta-blockers, diuretics and digitalis. Cardiac resynchronization therapy represents a novel option of treatment for only 25% of patients. Nevertheless the prognosis of patients with chronic heart failure with conventional medical therapy is remaining poor. Additional improvement in the treatment of patient with chronic heart failure remains a priority medical task. The results of this case report argues for CPAP as further adjunctive treatment option in patients with chronic heart failure.

[Cardiovascular end organ impairment due to hypertension]. / Kardiovaskuläre Endorganschäden des Hochdrucks.

Arterial hypertension is the most frequent cause of pressure overload on the left ventricle. Longer lasting arterial hypertension leads to hypertension-specific organ manifestations summarized as "hypertensive heart disease". Hypertensive heart disease comprise the manifestation of stenosis in epicardial arteries, hypertensive microvascular disease, ischemic cardiomyopathy, left ventricular hypertrophy, endothelial dysfunction, increased sympathetic drive and degeneration of aortic valve. Diastolic dysfunction and reduced coronary flow reserve can be evaluated as early markers of hypertensive heart disease. These alterations lead to the major clinical manifestations of hypertensive heart disease that are symptoms of reduced coronary insufficiency with typical angina pectoris, but also of symptoms of heart failure (systolic and diastolic dysfunction) and arrhythmia. Different non-invasive and invasive procedures are available for screening and follow-up of patients with hypertensive heart disease. Primary therapeutic target is, apart from lowering blood pressure, to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms.

Alterations of left ventricular function in women with insulin-dependent diabetes mellitus during pregnancy.

AIMS/HYPOTHESIS: During pregnancy, eminent cardiovascular changes occur. The aim of the following study was to investigate the course of haemodynamic parameters under the increased volume load during pregnancy and delivery in women with insulin-dependent diabetes mellitus. METHODS: We examined 51 pregnant diabetic women and 51 healthy pregnant women. The control group consisted of 51 healthy non-pregnant women. In all women, left ventricular mass and fractional shortening were calculated. To evaluate left ventricular diastolic function, mitral inflow and pulmonary venous flow profiles were analysed. RESULTS: During pregnancy left ventricular mass increased, fractional shortening decreased and diastolic dysfunction was found. While the healthy pregnant women developed signs of disturbed relaxation during pregnancy, pregnant diabetic women showed signs of a disturbed relaxation at the beginning of gestation. Of the pregnant diabetic women, 29 developed a restrictive filling pattern at the 24th week of gestation. The remaining 22 diabetic women had a comparable restrictive filling pattern only during vaginal delivery. In 10 of the 29 pregnant diabetic women dangerous complications were documented, while there were no complications in the healthy pregnant women and the other 22 diabetic pregnant women. CONCLUSION/INTERPRETATION: In healthy women pregnancy results in a reversible physiologic left ventricular hypertrophy, a disturbed relaxation pattern and a temporary decrease of left ventricular systolic function. In contrast, pregnant diabetic women showed a delayed relaxation at the beginning of pregnancy and developed a restrictive filling pattern. The early development of a restrictive filling pattern could indicate complications during delivery in pregnant diabetic women.

[Alterations of left ventricular systolic and diastolic function in pregnant women with insulin-dependent diabetes mellitus]. / Veränderungen der linksventrikulären systolischen und diastolischen Funktion bei Patientinnen mit insulinpflichtigem Diabetes mellitus in der Schwangerschaft. Eine prospektive Untersuchung mittels M-mode-Echokardiographie und Doppler-Echokardiographie.

BACKGROUND: During pregnancy, major cardiovascular changes occur. The aim of the following study was to investigate the course of hemodynamic parameters under the increased volume load during pregnancy and delivery in women with insulin-dependent diabetes mellitus. METHODS: We examined 51 pregnant diabetic and 51 healthy pregnant women. The control group consisted of 51 healthy non-pregnant women. In all women, left ventricular mass and fractional shortening were calculated. To evaluate left ventricular diastolic function, mitral inflow and pulmonary venous flow profiles were analyzed. RESULTS: During pregnancy left ventricular mass increased, fractional shortening decreased and diastolic dysfunction was found. While the healthy pregnant women developed signs of disturbed relaxation during pregnancy, pregnant diabetic women showed signs of a disturbed relaxation already at the beginning of gestation. A total of 29 pregnant diabetic women developed a restrictive filling pattern already at the 24th week of gestation. The remaining 22 diabetics had a comparable restrictive filling pattern only during vaginal delivery. In 10 of the 29 pregnant diabetic women dangerous complications were documented, while there were no complications in the healthy pregnant women and the other 22 diabetic pregnant women. CONCLUSIONS: In healthy women pregnancy results in a reversible physiologic left ventricular hypertrophy, a disturbed relaxation pattern and a temporary decrease of left ventricular systolic function. In contrast, pregnant diabetic women demonstrated a delayed relaxation at the beginning of pregnancy and developed a restrictive filling pattern. The early development of a restrictive filling pattern may predispose to complications during delivery in pregnant diabetic women.

Left ventricular diastolic dysfunction as an early manifestation of diabetic cardiomyopathy.

AIMS/HYPOTHESIS: Early determination of myocardial manifestations of diabetes mellitus is of major importance, since myocardial involvement considerably influences the prognosis of diabetic patients. The aim of this study was to investigate whether young patients with insulin-dependent diabetes mellitus and normal systolic left ventricular (LV) function already show a diastolic LV dysfunction and an increased risk of arrhythmias. METHODS: Echocardiography was performed in 87 patients suffering from type I diabetes mellitus, without known cardiac disease and in 87 controls. Patients with a known manifest cardiac disease or a long-term diabetic syndrome were excluded. Morphological parameters were determined using M-mode echocardiography. Doppler echocardiography was used to evaluate parameters of LV diastolic function. The risk of arrhythmia was assessed by means of electrocardiography, heart rate variability, and late potential analysis. RESULTS: The left atrial and ventricular dimensions and systolic functional parameters of all patients were normal. A diastolic dysfunction with a reduction in early diastolic filling, an increase in atrial filling, an extension of isovolumetric relaxation and deceleration time was documented in diabetic patients, as well as an increased number of supraventricular and ventricular premature beats. CONCLUSION: Even young patients with diabetes mellitus suffer from a diastolic dysfunction while systolic ventricular function is normal. Therefore, echocardiography with measurements of diastolic functional parameters appears to be a sensitive method for evaluating the manifestation and course of early diabetic cardiomyopathy.

[Left ventricular diastolic function parameters after PTCA and stent implantation]. / Linksventrikuläre diastolische Funktionsparameter nach PTCA und Stentimplantation.

UNLABELLED: This study was designed to determine the effect of successful coronary revascularisation on left ventricular diastolic function. METHODS: We consecutively studied the time course of diastolic function by Doppler echocardiography in 100 patients with one-vessel disease before and 48 hours after elective coronary angioplasty. Three abrupt vessel closures occurred within 24 hours after intervention. These three patients were excluded from the study. 58 patients were initially successful treated with coronary angioplasty (residual stenosis < 40%). In 39 patients stents were used to improve an inadequate result after coronary angioplasty. The following parameters of left ventricular diastolic function were evaluated before and 48 hours after coronary intervention: peak early (VE, m/s) and peak late diastolic (VA, m/s) flow velocity, E/A ratio, acceleration time (AT, ms), deceleration time (DT, ms) and isovolumetric relaxation time (IVRT, ms). Ejection fraction (EF; %) was determined and used to characterise systolic left ventricular function. RESULTS: Both patient groups (58 patients with coronary angioplasty and 39 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 revascularisation. Surprisingly there was no significant short-term improvement (48 hours) of diastolic function in patients with initially successful angioplasty. CONCLUSION: We suppose that stent implantation faster normalises coronary blood flow than coronary angioplasty.

Morphological differences of the internal thoracic artery in patients with and without coronary artery disease--evaluation by duplex-scanning.

OBJECTIVE: The internal thoracic artery is an established arterial graft for myocardial revascularisation, especially of the left anterior descending artery because of a higher patency rate compared to venous grafts. It has never been investigated, whether there are morphological differences in this vessel between patients with or without coronary artery disease or if they are comparable to morphological changes in the common carotid artery. METHODS: We investigated the internal thoracic artery and the common carotid artery of 24 patients (12 with coronary artery disease, 12 without coronary artery disease) with an ultrasonic system on both sides. The intima-media thickness and the diameter of both vessels were estimated. RESULTS: The intima-media-thickness of the internal thoracic artery was comparable in all patients, independent of the presence of a coronary artery disease (0.51+/-0.11 mm with coronary artery disease, 0.50+/-0.17 mm without coronary artery disease, P>0.05). Compared with this the intima-media-thickness of the common carotid artery was thicker in patients with coronary artery disease (0.84+/-0.13 mm with coronary artery disease, 0.73+/-0.07 mm without coronary artery disease, P< or or =0.014). There was no correlation between the thickness of the internal thoracic artery and the common carotid artery (r=0.018, P>0.05). CONCLUSIONS: It could be demonstrated for the first with non-invasive ultrasound, that the intima-media-complex of the internal thoracic artery is protected of the influence of arteriosclerosis. There are no morphological differences like the intima-media-thickness of the common carotid artery. The proven protective mechanism underlines the widespread use of the internal thoracic artery as a coronary artery bypass graft.

[Left ventricular diastolic function in pregnancy in patients with arterial hypertension. A prospective study with M-mode echocardiography and Doppler echocardiography]. / Linksventrikuläre diastolische Funktion in der Schwangerschaft bei Patientinnen mit arterieller Hypertonie. Eine prospektive Untersuchung mittels M-mode-Echokardiographie und Doppler-Echokardiographie.

INTRODUCTION: During pregnancy eminent cardiovascular changes occur. The aim of the following study was to investigate the course of hemodynamic parameters under increased volume load during pregnancy in women suffering from mild arterial hypertension. METHODS: Altogether 47 women (age: 25 +/- 4 years) with mild arterial hypertension detected during pregnancy underwent echocardiography at the 9th, 24th and 33rd week of gestation. Furthermore echocardiography was performed postpartum at weeks 1 and 8. The control group comprised 45 healthy pregnant women. In all patients left ventricular muscle mass index and systolic shortening fraction were measured. The following Doppler echocardiographic parameters were ascertained: peak early diastolic and peak late diastolic flow, VE/VA ratio, acceleration time, deceleration time and isovolumetric relaxation time. RESULTS: During pregnancy all patients had an increase of left ventricular muscle mass index and a decrease of fractional shortening. All patients developed a relevant diastolic dysfunction. While the control group developed signs of disturbed relaxation as reduction of peak early diastolic flow (0.89 +/- 0.07 versus 0.82 +/- 0.08 m/s*), VE/VA ratio and an increase of isovolumetric relaxation time (72 +/- 12 versus 123 +/- 7*) at the 33rd week of gestation (* p < 0.01), all pregnant women with mild arterial hypertension developed a diastolic dysfunction with signs of delayed relaxation already at the beginning of gestation. 26 pregnant women with arterial hypertension developed a restrictive diastolic filling pattern at 24 weeks of gestation. The other 21 pregnant women only showed restriction for a short time at the end of gestation. In healthy pregnant women, volume load results in a reversible physiologic left ventricular hypertrophia, a significant alteration of diastolic left ventricular function in terms of a disturbed relaxation pattern and a temporary decrease of systolic function. In comparison hypertensive pregnant women show a delayed relaxation at the beginning of pregnancy and 50% developed early signs of restrictive cardiomyopathy. These changes may predispose to critical complications during pregnancy.