Hendrik B Schmidt

Publications (4)12.55 Total impact

• Article: Risk stratification in patients with chronic heart failure based on metabolic-immunological, functional and haemodynamic parameters.

  Ralph Herrmann, Anja Sandek, Stephan von Haehling, Wolfram Doehner, Hendrik B Schmidt, Stefan D Anker, Mathias Rauchhaus
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  ABSTRACT: A vast array of parameters has been proposed to predict mortality in chronic heart failure (CHF). Their applicability into clinical practice remains challenging due to economical and availability considerations. We studied serum uric acid, total cholesterol, and soluble tumour necrosis factor receptor 1 (sTNF-R1) in 114 CHF patients (63.0 ± 1.0 years, NYHA functional class I/II/III/IV: 11/34/54/15) recruited prospectively into a metabolic study program. All patients underwent assessment of left ventricular ejection fraction and measurement of peak oxygen consumption (pVO(2)). Patients were followed for 24 months or until death. A total of 31 patients died; cumulative survival was 78% (95% confidence interval [CI] 70-86%) and 73% (65-81%) at 12 and 24 months, respectively. In single predictor Cox proportional hazard analysis, uric acid, pVO2, sTNFR-1, LVEF (all p<0.0001) and cholesterol (p<0.02) all predicted survival. All parameters remained significant predictors of death after multivariable adjustment (all p<0.02). Receiver-operator characteristic (ROC) curve analyses showed that uric acid and sTNF-R1 are equally strong with regards to their prognostic performance in CHF like pVO(2,) but even better than LVEF. The combination of pVO(2), LVEF, uric acid, and sTNF-R1 in ROC statistics turned out as the best model with the highest prognostic value in CHF (AUC: 0.91, sensitivity: 90.4, specificity: 74.2, p=0.0001). Including metabolic-immunological parameters into risk assessment might result in a better risk stratification than modeling based on clinical parameters alone, probably due to a better reflection of CHF as multisystem disease. We suggest metabolic-immunological parameters to be tested in larger populations.
  International journal of cardiology 11/2010; 156(1):62-8. · 7.08 Impact Factor
• Article: The impact of impaired renal function on mortality in patients with acutely decompensated chronic heart failure.

  Amalia Vaz Pérez, Katrin Otawa, Arabel V Zimmermann, Martin Stockburger, Ursula Müller-Werdan, Karl Werdan, Hendrik B Schmidt, Hüseyin Ince, Mathias Rauchhaus
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  ABSTRACT: Acute heart failure syndromes, commonly recognized as de novo heart failure or acute decompensated chronic heart failure (ADHF), are characterized by a rapid onset or change in signs and symptoms of heart failure requiring urgent treatment. Coexisting renal dysfunction is associated with poor prognosis in these patients. We sought to determine whether renal impairment in particular and other admission factors in general predict long-term mortality after hospitalization for ADHF. We studied 128 patients (age 63 + or - 12 years, 76% male) in NYHA class 2.6 + or - 0.7 with a left ventricular ejection fraction (LVEF) < or = 39%, hospitalized due to ADHF. Mortality rates (per 100 person-years) were 21.9 at 12 months and 12.0 at 60 months. We found that admission serum creatinine level was the best predictor of mortality after 1 (P < 0.001, log-transformed due to skewed distribution) and 5 years (P = 0.001), followed by creatinine clearance, the use of loop diuretics, and digoxin. Moreover, higher NYHA class, decreased body mass index (BMI) and increased levels of urea predicted 1 and 5 years mortality on univariate analysis. In the multivariate analysis, creatinine, NYHA class, and LVEF emerged as independent predictors of mortality after 1 year, whereas BMI and the use of diuretics did not reach significance (joint chi(2) = 29.40, P < 0.001). After 5 years, creatinine and NYHA class independently predicted all-cause mortality (joint chi(2) = 22.71, P < 0.001), but BMI and age did not remain significant. Admission creatinine level strongly predicts medium- and long-term mortality after hospitalization in patients with ADHF, and serves as a cheap and fast clinical marker to identify patients at risk of death.
  European Journal of Heart Failure 02/2010; 12(2):122-8. · 4.90 Impact Factor
• Article: Septic cardiomyopathy - A not yet discovered cardiomyopathy?

  Ursula Muller-Werdan, Michael Buerke, Henning Ebelt, Konstantin M Heinroth, Anja Herklotz, Harald Loppnow, Martin Ruß, Frithjof Schlegel, Axel Schlitt, Hendrik B Schmidt, Gerold Söffker, Karl Werdan
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  ABSTRACT: Myocardial depression in human sepsis was only unequivocally proven in the 1980s by the group of Parrillo, who used nuclear imaging techniques to measure heart volumes and function in intensive care patients. Heart failure in sepsis is frequently masked by a seemingly normal cardiac output. However, relative to the lowered systemic vascular resistance - resulting in a reduced afterload - cardiac outputs and ventricular ejection fractions are often not adequately enhanced. This septic cardiomyopathy (impairment of the heart within the scope of systemic sepsis) involves both the right and the left ventricles, and is potentially reversible. In response to volume substitution, the heart can be considerably enlarged. The cardiomyopathy is not primarily hypoxic in nature, but may be aggravated by ischemia. Autonomic dysfunction, documented by a reduced heart rate variability and impaired baroreflex and chemoreflex sensitivities, forms part of the disease entity. The severity of myocardial depression correlates with a poor prognosis. Noninfectious systemic inflammatory response syndrome can give rise to an analogous disease entity, namely, systemic inflammatory response syndrome cardiomyopathy.The etiology of septic cardiomyopathy is multifactorial. Several candidates with a potential pathogenetic impact on the heart were identified: bacterial toxins; cytokines and mediators including tumour necrosis factor-alpha, interleukin-1 and nitric oxide; cardiodepressant factors; oxygen reactive species; and catecholamines. Symptomatic treatment consists of volume substitution and catecholamine support; causal therapeutic approaches aiming at an interruption of the proinflammatory mediator cascades are being tested.
  Experimental and clinical cardiology 01/2006; 11(3):226-36. · 0.58 Impact Factor
• Chapter: Septic Cardiomyopathy

  Karl Werdan, Hendrik B. Schmidt, Frithjof Schlegel, Anja Herklotz, Ursula Mueller-Werdan
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  ABSTRACT: The existence of human septic myocardial depression was only unequivocally proven in the 1980s by the group of Parrillo, utilizing a nuclear imaging technique in intensive care patients. Heart failure in sepsis is frequently masked by a seemingly normal cardiac output. However, relative to the lowered systemic vascular resistance—resulting in a reduced afterload, cardiac outputs and ventricular ejection fractions of septic patients are often not adequately enhanced. This septic cardiomyopathy involves both the right and the left ventricle and is potentially reversible. In response to volume substitution, the hearts can be considerably enlarged. The disease is not primarily hypoxic in nature, but may be aggravated by ischemia. Autonomic dysfunction, documented by a reduced heart rate variability and impaired baro– and chemoreflex sensitivities, forms part of the disease entity. The severity of myocardial depression correlates with a poor prognosis. Non-infectious systemic inflammatory response syndrome (SIRS) can give rise to an analogous disease entity, namely SIRS cardiomyopathy. The etiology of the disease is multifactorial. Several candidates with potential pathogenic impact on the heart were identified: bacterial toxins, cytokines and mediators including tumor necrosis factor α, interleukin-1 and nitric oxide, cardiodepressant factors, oxygen reactive species, catecholamines. Symptomatic treatment consists of volume substitution and of catecholamine support; causal therapeutic approaches aiming at an interruption of the proinflammatory mediator cascades are being tested. Key wordsCardiomyopathy–septic—Sepsis—Autonomic dysfunction—Shock–septic—Heart failure–septic
  12/2002: pages 3-21;