Effects of Exercise and Ischemia on Mobilization and Functional Activation of Blood-derived Progenitor Cells in Patients with Ischemic Syndromes: Results of 3 Randomized Studies

Circulation. Jun, 2005  |  Pubmed ID: 15956121

Exercise training (ET) has been shown to improve regional perfusion in ischemic syndromes. This might be partially related to a regeneration of diseased endothelium by circulating progenitor cells (CPCs) or CPC-derived vasculogenesis. The aim of the present study was to determine whether ischemic stimuli during ET are required to promote CPC mobilization in patients with cardiovascular diseases.

[Acute Heart Failure: Rational Diagnostics in Clinical Practice and the Emergency Department]

Herz. Nov, 2006  |  Pubmed ID: 17149675

Despite being as common as an acute myocardial infarction in the emergency department, the diagnostic criteria and the therapeutic guidelines for heart failure treatment are much less well defined. Thanks to the recently published guidelines of the European Society of Cardiology (ESC) the diagnosis of acute heart failure syndromes (AHFS) is now better standardized. The ESC distinguishes between six AHFS: (I) acute decompensated chronic heart failure, (II) acute heart failure with hypertension/hypertensive crisis, (III) acute heart failure with pulmonary edema, (IV) cardiogenic shock, (V) high-output failure, and (VI) right-sided acute heart failure. To distinguish between these entities in a clinical setting, a well-structured clinical examination is of paramount importance. Signs of peripheral hypoperfusion and congestion/fluid overload need to be recognized rapidly. These two clinical parameters permit the assessment of the patient based on the Clinical Severity Classification. Further diagnostic work-up should include chest X-ray, echocardiography, clinical chemistry, and blood gas analysis. The invasive coronary angiography is only beneficial in the context of an acute ST elevation myocardial infarction or NSTEMIs with persistent symptoms of angina. In all other cases cardiac catheterization should be deferred until the patient is recompensated. Diagnostic algorithms help to maintain a high standard in clinical diagnosis and improve the safety and efficacy of subsequent therapeutic interventions.

Prognostic Value of Heart Rate Increase at Onset of Exercise Testing

Circulation. Jan, 2007  |  Pubmed ID: 17242274

The initial response of heart rate to dynamic exercise has been proposed as having prognostic value in limited studies that have used modalities other than the treadmill. Our aim was to evaluate the prognostic value of early heart rate parameters in patients referred for routine clinical treadmill testing.

The Prognostic Value of T Wave Amplitude in Lead AVR in Males

Annals of Noninvasive Electrocardiology : the Official Journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. Apr, 2008  |  Pubmed ID: 18426436

Since there is an uncertainty regarding which of the 12 leads provides the most information, we investigated the association between repolarization phenomenon in all of the 12 leads and cardiovascular (CV) mortality.

Comments on Point: Counterpoint: Exercise Training Does/does Not Induce Vascular Adaptations Beyond the Active Muscle Beds

Journal of Applied Physiology (Bethesda, Md. : 1985). Sep, 2008  |  Pubmed ID: 18800399

A Simplified Clinical Electrocardiogram Score for the Prediction of Cardiovascular Mortality

Clinical Cardiology. Feb, 2009  |  Pubmed ID: 19215007

Electrocardiogram (ECG) scores have been demonstrated to predict CV mortality but they are rarely utilized clinically.

Risk Factor Management: Antiatherogenic Therapies

European Journal of Cardiovascular Prevention and Rehabilitation : Official Journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology. Aug, 2009  |  Pubmed ID: 19675434

Despite the advances in interventional techniques, the management of stable atherosclerosis remains the domain of optimal guideline-oriented therapy. Recent studies on the effects of aggressive lipid lowering on atheroma volume changes using intravascular ultrasound indicate that it is possible to achieve atherosclerosis regression by reaching low-density lipoprotein (LDL) levels less than 75 mg/dl. The pleiotropic anti-inflammatory effects of statins contribute to the reduction of cardiovascular (CV) event observed with aggressive lipid lowering. As a second important strategy to prevent disease progression, lifestyle changes with regular physical exercise are capable of halting the atherosclerotic process and reducing angina symptoms and CV events. Optimal medical therapy, a healthy lifestyle with regular physical exercise, and coronary interventions are not mutually exclusive treatment strategies. Over the last few decades, both have proved to be effective in significantly reducing the CV mortality in the Western world. However, risk factor modification contributed to at least half the effect in the reduction of CV mortality. This figure provides an estimate of what could be achieved if we were to take risk factor modification more seriously - especially in the acute care setting. The knowledge is there: today we have a better understanding on how to stop progression and even induce regression of atherosclerosis. Much research still needs to be done and will be done. In the meantime, however, our primary focus should lie in implementing what is already known. In addition, it is essential not just to treat CV risk factors, but also to treat them to achieve the target values as set by the guidelines of European Society of Cardiology.

Exercise Training in Patients with Advanced Chronic Heart Failure (NYHA IIIb) Promotes Restoration of Peripheral Vasomotor Function, Induction of Endogenous Regeneration, and Improvement of Left Ventricular Function

Circulation. Heart Failure. Jul, 2010  |  Pubmed ID: 20430934

Attenuated peripheral perfusion in patients with advanced chronic heart failure (CHF) is partially the result of endothelial dysfunction. This has been causally linked to an impaired endogenous regenerative capacity of circulating progenitor cells (CPC). The aim of this study was to elucidate whether exercise training (ET) affects exercise intolerance and left ventricular (LV) performance in patients with advanced CHF (New York Heart Association class IIIb) and whether this is associated with correction of peripheral vasomotion and induction of endogenous regeneration.

Maximal Exercise, Limb Ischemia, and Endothelial Progenitor Cells

European Journal of Cardiovascular Prevention and Rehabilitation : Official Journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology. Feb, 2011  |  Pubmed ID: 20571405

The concept of neovascularization in response to tissue ischemia was recently extended by the finding of postnatal vasculogenesis through circulating endothelial progenitor cells (EPCs). The aim of this study was to assess the role of acute ischemia for EPC mobilization in patients with peripheral arterial occlusive disease (PAOD) and in healthy volunteers.

Exercise-induced Modulation of Endothelial Nitric Oxide Production

Current Pharmaceutical Biotechnology. Sep, 2011  |  Pubmed ID: 21235458

In the arterial wall nitric oxide (NO) is the key transmitter for endothelium-dependent regulation of vascular tone. It is produced in intact endothelial cells by endothelial NO synthase (eNOS) as the key enzyme from L-arginine. Endothelial NO generation is highly regulated by mechanical, humoral, and metabolic factors. The regulation of NO synthesis occurs at different levels: ENOS gene polymorphisms are related to eNOS expression and activity and may potentially increase coronary event rate, mRNA expression is influenced by estrogen status and shear stress, mRNA stability is enhanced by vascular endothelial growth factor (VEGF), and final enzyme activity is regulated by the phosphorylation status at serine/threonine residues. Released from endothelial cells NO is rapidly transported to the neighboring vascular smooth muscle cells (VSMCs), where it induces the production of cGMP as a second messenger. CGMP in turn increases Ca2+ uptake into intracellular calcium stores thereby lowering [Ca2+]i and inducing VSMC relaxation and vasodilation. On its way to the VSMCs NO may be prematurely degraded by reactive oxygen species. On the other hand, chronic endurance exercise with regular bouts of increased laminar flow along the endothelium has the potential to increase eNOS mRNA expression and phosphorylation via AKT (protein kinase B) and to reduce oxidative stress by improving antioxidative protection. The growing knowledge about the complex regulation of NO synthesis and degradation in cardiovascular diseases and its response to exercise has led to a new understanding of the protective effects of long-term habitual physical activity against atherosclerotic heart disease and vascular aging.

Exercise Training Leads to a Reduction of Elevated Myostatin Levels in Patients with Chronic Heart Failure

European Journal of Cardiovascular Prevention and Rehabilitation : Official Journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology. Mar, 2011  |  Pubmed ID: 21450574

Background: In chronic heart failure (CHF), cardiac cachexia is often associated with the terminal stage of this disease. In animal studies it has been demonstrated that myostatin, a key regulator of skeletal muscle mass, is elevated in advanced stages of this syndrome. Design: The aim of the present study was to investigate the expression of myostatin in patients with late stage CHF (NYHA IIIb) in comparison to healthy subjects. Furthermore the effects of physical exercise on myostatin were analyzed. Methods: Twenty-four patients were either randomized to a sedentary control group (CHF-S) or exercise training (CHF-E). At baseline and after 12 weeks mRNA and myostatin protein in the peripheral skeletal muscle as well as myostatin serum concentration were measured. Furthermore 12 age-matched healthy men were compared to all patients at baseline (HC). Results: CHF patients showed a two-fold increase of myostatin mRNA (p = 0.05) and a 1.7-fold (p = 0.01) augmentation of protein content in skeletal muscle compared to healthy subjects. In late-stage CHF, exercise training led to a 36% reduction of the mRNA and a 23% decrease of the myostatin protein compared to baseline. The serum concentration of myostatin revealed no significant alteration between the groups. Conclusion: In the skeletal muscle, myostatin increases significantly in the course of CHF. The observed effects of a significant reduction of myostatin in skeletal muscle after 12 weeks of exercise training demonstrate the reversibility of molecular changes that might be able to halt the devastating process of muscle wasting in chronic heart failure.

[Conservative Management of Coronary Artery Disease]

MMW Fortschritte Der Medizin. Sep, 2011  |  Pubmed ID: 21977795

The Leipzig Prospective Vascular Ultrasound Registry in Radial Artery Catheterization: Impact of Sheath Size on Vascular Complications

JACC. Cardiovascular Interventions. Jan, 2012  |  Pubmed ID: 22230148

This study investigated the impact of sheath size on the rate of radial artery occlusions (RAO) (primary objective) and other access site complications (hemorrhage, pseudoaneurysm, arteriovenous fistula) as secondary objectives after transradial coronary catheterization.

Age-related Effects of Exercise Training on Diastolic Function in Heart Failure with Reduced Ejection Fraction: The Leipzig Exercise Intervention in Chronic Heart Failure and Aging (LEICA) Diastolic Dysfunction Study

European Heart Journal. Jan, 2012  |  Pubmed ID: 22267243

AimsDiastolic dysfunction (DD) was identified as a predictor of adverse prognosis in heart failure with reduced ejection fraction (HFREF). It is, however, unknown if DD is improved by exercise training, which is known to induce reverse remodelling, and if the training effect is attenuated in elderly HFREF patients. We therefore assessed DD in a cohort of referent controls (RCs) and HFREF patients and studied the response of DD to endurance exercise in two age groups (≤55 years and ≥65 years).Methods and resultsSixty RC (30 ≤ 55 years, mean age 50 ± 5 years; 30 ≥ 65 years, 72 ± 4 years) and 60 HFREF patients (30 ≤ 55 years, 46 ± 5 years; 30 ≥ 65 years, 72 ± 5 years, EF 28 ± 5%) were randomized to 4 weeks of supervised endurance training or to a control group. Exercise training was effective in reducing LV isovolumetric relaxation time by 29% in young and by 26% in old HFREF patients (P< 0.05 for both). As assessed by tissue Doppler, septal E' increased by 37% in young and by 39% among old HFREF patients (P< 0.005 for both) resulting in a significant decrease in the E/E' ratio from 13 ± 1 to 10 ± 1 in young and 14 ± 1 to 11 ± 1 in old HFREF patients (P< 0.05 for both). Serum levels of N-terminal pro brain natriuretic peptide were significantly reduced after endurance training in HFREF patients of all ages.ConclusionIn HFREF, diastolic function is significantly impaired in all age groups. Endurance training is highly effective in improving left ventricular diastolic function in HFREF patients regardless of age.This study is registered at ClinicalTrials.gov (number: NCT00176319).