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Biomedical subjects

Martin Hülsmann

Publications and source records attributed to Martin Hülsmann.

9 recordsLinked to original sources
PubMed2005

Flow-mediated vasodilation predicts outcome in patients with chronic heart failure: comparison with B-type natriuretic peptide.

OBJECTIVES: The aim of this study was to assess the predictive potency of impaired endothelium-dependent flow-mediated vasodilation (FMD) in patients with chronic heart failure (CHF). BACKGROUND: Chronic heart failure is associated with reduced FMD; the prognostic impact of this observation is unknown. METHODS: Seventy-five ambulatory CHF patients (United Network of Organ Sharing [UNOS] status 2) with a left ventricular ejection fraction (LVEF) < or =30%, despite optimized medical therapy (angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, 100%; beta-blocker, 81%), were evaluated. Using high-resolution ultrasound, FMD of the brachial artery was assessed in addition to other neurohormonal, clinical, and hemodynamic variables. Age, gender, New York Heart Association (NYHA) functional class, LVEF, hemodynamic variables, B-type natriuretic peptide (BNP) levels, medical therapy, cardiovascular risk factors, and FMD were analyzed for prediction of the combined end point conversion to UNOS status 1 or death in a multivariate Cox model. RESULTS: Up to three years, 21 patients (28%) converted to UNOS status 1, and 6 patients (8%) died. Univariate risk factors for the combined end point were log BNP (p = 0.0032), FMD (p = 0.0033), NYHA functional class (p = 0.0132), beta-blocker therapy (p = 0.0367), and mean blood pressure (p = 0.0406). In the multivariate analysis, only FMD (p = 0.0007), log BNP (p = 0.0032), and mean blood pressure (p = 0.0475) were independently related to the combined end point. In the Kaplan-Meier plot, significantly more patients with FMD <6.8% (median) reached the combined end point, as compared with patients with FMD >6.8% (p = 0.004). CONCLUSIONS: In CHF, impaired FMD is a strong, independent predictor of conversion to UNOS status 1 or death.

Adult↗
PubMed2005

Dynamics of inflammation parameters prior to tachyarrhythmias in critically ill patients.

BACKGROUND: The aim of this study was to assess the dynamics of inflammation parameters prior to a tachyarrhythmic event in critically ill patients. We evaluated the course of inflammation parameters over 48 hours before the occurrence of tachyarrhythmias. METHODS: Prospective observational study conducted at a cardiologic medical-postoperative tertiary intensive care unit at the Vienna university hospital. Between November 1996 and July 1999 all consecutive patients (n = 756) were screened for the occurrence of arrhythmias. Patients with sustained tachyarrhythmias (n = 119) form the basis of the report. The tachyarrhythmia episodes were related to the evolution of C-reactive protein, leukocytes and fibrinogen during the 48 hours before the arrhythmic event. RESULTS: A total of 278 tachyarrhythmia episodes was identified (wide QRS complex tachycardia, n = 168; narrow QRS complex tachycardia, n = 108; ventricular fibrillation, n = 2). The body temperature on the day of arrhythmia was 37.4 +/- 1 degrees C. Overall, there was no statistically significant change in any inflammation parameter within 48 hours prior to tachyarrhythmias (C-reactive protein: 17.4 +/- 12 [-48 h], 16.2 +/- 11 [-24 h], 15.2 +/- 12 [0 h] mg/dl, p = 0.2). When stratifying for different levels of C-reactive protein on the day of arrhythmia, the trend was inhomogenous. For lower strata, values were significantly decreasing towards arrhythmias; for higher strata, an increase in C-reactive protein was observed (stratum A: 8.5 +/- 7.2 [-48 h], 6.6 +/- 4.9 [-24 h], 4.8 +/- 2.9 mg/dl [0 h], p = 0.0001; stratum B: 16.0 +/- 7.1 [-48 h], 13.8 +/- 6.0 [-24 h], 14.4 +/- 2.6 mg/dl [0 h], p = 0.09; stratum C: 21.2 +/- 7.4 [-48 h], 21.5 +/- 7.5 [-24 h], 24.9 +/- 3.0 mg/dl [0 h], p = 0.008; stratum D: 34.3 +/- 13.4 [-48 h], 35.7 +/- 9.0 [-24 h], 39.7 +/- 5.5 mg/dl [0 h], p = 0.13). CONCLUSION: In this group of critically ill patients inflammation parameters did not change significantly during the 48 hours prior to the arrhythmic event. For different levels of C-reactive protein at the time of arrhythmia, no clear dynamics of inflammatory signs were observed.

Aged↗
PubMed2005

Influence of age and in-patient care on prescription rate and long-term outcome in chronic heart failure: a data-based substudy of the EuroHeart Failure Survey.

AIMS: To evaluate the prescription rate of neurohumoral drugs in chronic heart failure patients and the factors influencing prescription rates. Outcomes and their predisposing factors were also investigated. METHODS AND RESULTS: Of 1482 consecutive patients admitted to 3 Austrian hospitals participating in the EuroHeart Failure Survey, 341 were included in this data-based substudy. Follow-up time to evaluate outcome was up to 46 months. The prescription rates of renin-angiotensin (RAAS) antagonists and beta-blockers at the time of discharge were evaluated. The overall prescription rate and dosage were lower than the recommended levels. Hospitals with cardiac care had a significantly higher prescription rate than those without (p<0.001). Patients older than 75 years received significantly less therapy (p<0.001) and a lower dosage of RAAS antagonists (p<0.01) than younger patients. Younger patients were treated more intensively in hospitals with cardiac care (p<0.05). Patients aged >75 years were under-treated, independent of the hospital (n.s.). Multivariate analysis showed that age was the most influencing factor on survival (chi(2) 15.5, p<0.0001). Additional influencing factors of long-term survival were type of the ward (chi(2) 7.9, p<0.005) and pharmacologic treatment (chi(2) 6.2, p<0.02). CONCLUSION: Patients with chronic heart failure are still under-treated in clinical practice. Younger patients benefit from hospitals with specialized cardiac care. Elderly patients are obviously under-treated compared with younger patients. Of several clinical parameters, age was the only independent variable predicting long-term survival.

Adrenergic beta-Antagonists↗
PubMed2005

Incidence of normal values of natriuretic peptides in patients with chronic heart failure and impact on survival: a direct comparison of N-terminal atrial natriuretic peptide, N-terminal brain natriuretic peptide and brain natriuretic peptide.

AIMS: N-ANP, N-BNP and BNP are proven to be excellent markers for diagnosis and the prediction of outcome in heart failure patients. Published studies on this subject differ in respect of their design and are therefore difficult to compare. The EuroHeart Failure Survey was undertaken to evaluate the drug prescription rate; the cohort of this survey best reflects clinical practice. The purpose of the present study was to compare the three hormones in clinical practice for the purpose of diagnosis and the prediction of outcome. Attention was focused on patients with normal values and the implications of these on survival. METHODS AND RESULTS: Of 341 patients recruited in the Austrian centers of the survey, blood samples for the determination of N-ANP, N-BNP and BNP were taken from 112 patients. Mortality within the observation period was defined as the endpoint. Normal levels of the hormones were found in 5% of cases for N-ANP, 25% for N-BNP and 30% for BNP. The mortality of patients with normal values was low (0%, 3% and 6%, respectively) and occurred late (after more than 23 months). Above-median levels of all three hormones resulted in a comparable mortality (51% survival for N-ANP, 50% for BNP and 49% for N-BNP). CONCLUSIONS: In a clinical setting, the risk stratification for outcome is similar for N-ANP, N-BNP and BNP. More importantly, all hormones are reliable parameters to diagnose CHF using normal values as a cut-point. However, N-ANP appears to be more sensitive than BNP or N-BNP.

Aged↗
PubMed2004

Muscle strength as a predictor of long-term survival in severe congestive heart failure.

AIMS: The objective of the study was to test the relationship between isolated muscle strength and outcome, and its significance in the context of other exercise variables. METHODS AND RESULTS: 122 consecutive patients (LVEF 21+/-7%) were enrolled in the study. Isokinetic strength testing of the knee extensor and flexor muscles were performed. A subset of 51 patients underwent additional upright bicycle testing with gas exchange analysis. The outcome up to 60 months was defined by event-free survival (group A, n=59) or death (group B, n=34). Patients who had been transplanted were excluded from further analysis. The peak strength of the quadriceps muscle was comparable in both groups (N.S.). In contrast, the index (value adjusted for weight) did reveal significant differences (P<0.04), similar to the peak torque of the knee flexor muscle (P<0.04), whose index was even more significant with regard to differences (P<0.01). Multivariate analysis including muscle strength variables, pVO2 and workload into one model show that the flexor strength index is the only independent variable (x2=9 P<0.003). A cut-off point of 68 Nm x 100/kg in the strength index of the flexor muscles was used to establish a significant difference between groups with regard to outcome (P<0.01). Thus, the isokinetic strength of the knee flexor muscles is related to outcome. Moreover, this parameter is superior to variables such as peakVO2 and workload.

Aged↗
PubMed2004

Interleukin-6 and B-type natriuretic peptide are independent predictors for worsening of heart failure in patients with progressive congestive heart failure.

BACKGROUND: Neurohormones and cytokines have been associated with poor prognosis in patients with congestive heart failure. However, direct comparisons between them are rare and the best predictor for worsening of heart failure remains to be elucidated. The aim of the study was to identify independent predictors for worsening of heart failure. METHODS: We studied 100 patients with congestive heart failure (LVEF <or=25%). Serum levels of interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, aminoterminal atrial natriuretic peptide (N-ANP), B-type natriuretic peptide (BNP), aminoterminal B-type natriuretic peptide (N-BNP), norepinephrine (NE) and big endothelin (big ET) were measured at entry into the study. Univariate and stepwise multivariate regression analyses were performed to compare variables and clinical parameters. The end-point was defined as worsening of heart failure. RESULTS: During follow-up (mean 378 days), 30 patients reached the defined end-point. Univariate risk factors of worsening of heart failure were IL-6 (p = 0.0001), log BNP (p = 0.0001), log N-ANP (p = 0.0259), big ET (p = 0.0032), log N-BNP (p = 0.0495), NE (p = 0.0013) and LVEF (p = 0.0498). Multivariate regression analysis identified IL-6 as the strongest independent predictive value for worsening of heart failure (p = 0.0001), followed by log BNP (p = 0.0002). Mean IL-6 levels were 1.76 +/- 1.73 in stable patients and 4.62 +/- 7.98 pg/ml in patients who developed worsening of heart failure. Using a cut-off value of 1.66 pg/ml for IL-6 Kaplan-Meier freedom from worsening, heart failure was significantly higher in patients below this cut-off point compared with those above (p = 0.0002). CONCLUSIONS: IL-6 and BNP independently predict worsening of heart failure. A single measurement could help to identify patients at high risk for worsening of heart failure and these individuals should be monitored more closely.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

NF449, a novel picomolar potency antagonist at human P2X1 receptors.

The antagonistic effects of the novel suramin analogue 4,4',4",4"'-(carbonylbis(imino-5,1,3-benzenetriylbis(carbonylimino)))tetrakis-benzene-1,3-disulfonic acid (NF449) were analyzed at homomeric human P2X(1) and P2X(7) receptor subtypes (hP2X(1) and hP2X(7)) heterologously expressed in Xenopus oocytes using the two-microelectrode voltage-clamp technique. At activating ATP concentrations of 1 microM (hP2X(1)) and 100 microM (hP2X(7)), IC(50) values of 0.05 nM and 40 microM were found for hP2X(1) and hP2X(7) receptors, respectively. The Schild analysis revealed a pA(2) of 10.7 at hP2X(1). Wash-in and wash-out of 10 nM NF449 were nearly complete within 16 s and 4 min, respectively, at the hP2X(1) receptor. An increase in the activating ATP concentration to 100 microM shifted the NF449 concentration-inhibition curve rightwards for the hP2X(1) receptor. NF449 decelerated activation as well as desensitization of hP2X(1). It is concluded that NF449 acts as a reversible competitive antagonist at the hP2X(1) with much higher potency at hP2X(1) than at hP2X(7) receptors. NF449 may hence be excellently suited to discriminate between both receptors in native human tissues.

Animals↗
PubMed2002

Hypertrophic osteoarthropathy caused by PGE1 in a patient with congestive heart failure during cardiac rehabilitation.

Continuous chronic drug infusion with PGE1 via a portable pump and neuromuscular electrical stimulation (NMES) help to improve the quality of life in patients with severe chronic heart failure waiting for a donor heart, as both treatments can be performed at home. We report a 56-year-old woman suffering from severe chronic heart failure, who was referred for a cardiac rehabilitation program because of progressive muscle weakness and weight loss. Due to her underlying heart disease she was unable to perform voluntary exercise. NMES of both knee extensor muscles was started. Under simultaneous chronic drug infusion with PGE1 via a portable pump the patient developed clinical signs of hypertrophic osteoarthropathy, which prevented her from continuing the rehabilitation program. X-ray examinations and bone scans concurred with the diagnosis of secondary hypertrophic osteoarthropathy. After the PGE1 dose had been reduced, the clinical signs of the osteoarthropathy resolved and the patient was able to continue the rehabilitation program with no difficulty. This case report underlines the importance of being aware of the potential side effects of modern cardiac drugs in the complex treatment of patients waiting for a donor heart.

Alprostadil↗