Browsing by Author "Heusch, Gerd"

Objectives The aim of this analysis was to compare troponin- positive patients presenting to a chest pain unit (CPU) and undergoing coronary angiography with or without subsequent revascularization. Leading diagnosis, disease distribution, and short-term outcomes were evaluated. Background Chest pain units are increasingly implemented to promptly clarify acute chest pain of uncertain origin, including patients with suspected acute coronary syndrome (ACS). Methods A total of 11,753 patients were prospectively enrolled into the German CPU-Registry of the German Cardiac Society between December 2008 and April 2011. All patients with elevated troponin undergoing a coronary angiography were selected. Three months after discharge a follow-up was performed. Results A total of 2,218 patients were included. 1,613 troponin-positive patients (72.7 %) underwent a coronary angiography with subsequent PCI or CABG and had an ACS in 96.0 %. In contrast, 605 patients (27.3 %) underwent a coronary angiography without revascularization and had an ACS in 79.8 %. The most frequent non-coronary diagnoses in non-revascularized patients were acute arrhythmias (13.4 %), pericarditis/myocarditis (4.5 %), decompensated congestive heart failure (3.7 %), Takotsubo cardiomyopathy (2.7 %), hypertensive crisis (2.4 %), and pulmonary embolism (0.3 %). During the 3-month follow-up, patients without revascularization had a higher mortality (12.1 vs. 4.5 %, p < 0.0001) representing the major contributor to the higher rate of MACCE (15.1 vs. 8.1 %, p < 0.001). These data were confirmed in a subgroup analysis of ACS patients with or without revascularization. Conclusions Patients presenting to a CPU with elevated troponin levels mostly suffer from ACS and in a smaller proportion a variety of different diseases are responsible. The short-term outcome in troponin-positive patients with or without an ACS not undergoing a revascularization was worse, indicating that these patients were more seriously ill than patients with revascularization of the culprit lesion. Therefore, an adequate diagnostic evaluation and improved treatment strategies are warranted.

Background: Given the multimodal medical and interventional treatment options in coronary artery disease, the additional value of intensified lifestyle modification is unclear. We have therefore examined the effects of lifestyle modification on top of current treatment and also associated with the GNB3 C825T polymorphism, which has established association to sympathetic activation and the precipitation of angina. Methods: One hundred one patients with established coronary artery disease were randomized to a 1-year lifestyle modification group (lifestyle group [LG]) or an advice group. Risk factors, coronary calcification (electron beam tomography), heart rate variability, baroreflex sensitivity, anginal symptoms, and quality of life (QOL) were assessed on entry and after 1 year. Results: Patients in LG had excellent program adherence, but lifestyle modification had no impact on metabolic risk factors and coronary calcification. Changes in heart rate, heart rate variability, and blood pressure were only slightly favoring LG. Baroreflex sensitivity increased by 2 (0.79-3.13) ms/mm Hg in the LG but decreased by -0.10 (-1.11 to 0.92) in the advice group (P = .013). Lifestyle modification led to improved physical QOL, reductions of anginal attacks (-54% vs 11%, P = .01), and dose reductions in 30% of anti-ischemic medications (P = .004). 825T allele carriers had a more pronounced reduction of heart rate and improvement of angina and QOL. The beneficial effect on reduction of medication was seen in 825T allele carriers only. Conclusions: In the presence of modern treatments, comprehensive lifestyle modification provides no additional benefits on progression of atherosclerosis but improves autonomic function, angina, and QOL with concomitant reduced need of medication. These responses are more pronounced in GN83 825T allele carriers.

Background - The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction. Methods and Results - Microembolization was induced by injecting microspheres (42-mum diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (n = 7) or methylprednisolone 30 mg/kg IV either 30 minutes before (n = 7) or 30 minutes after (n = 5) microembolization. In addition, chronically instrumented dogs received either placebo (n = 4) or methylprednisolone (n = 4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0 +/- 2.1% (mean +/- SEM) at baseline to 5.8 +/- 0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0 +/- 0.7% at 4 to 6 hours after microembolization back to baseline (19.1 +/- 1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction. Conclusions - Methylprednisolone, even when given after microembolization, prevents progressive contractile dysfunction.

In an attempt to improve the treatment of patients with acute coronary syndromes (ACS), a network of certified chest pain units (CPUs) has been recently established in Germany. Data from patients admitted between December 2008 and September 2011 for ACS in 40 certified CPUs participating in the registry were prospectively collected. A total of 5,457 patients was admitted for ACS; 798 patients (14.6 %) were diagnosed with an ST-elevation myocardial infarction (STEMI), 2,244 (41.1 %) with a non-ST-elevation myocardial infarction (NSTEMI), and 2,415 (44.3 %) with unstable angina. The mean time to first medical contact was 2:08 h for STEMI patients. A pre-hospital ECG was available in 23.8 % of all ACS patients. Importantly, evidence of ST-segment elevation was present in 79.7 % of the STEMI patients already in this pre-hospital ECG. As many as 76.6 % of the patients, independently of their symptoms and final diagnosis, received an ECG within 10 min of reaching the CPU. 98.2 % of STEMI patients underwent invasive diagnostics, with an in-hospital delay as little as 31 (11-75) min. The establishment of a nation-wide network of certified CPUs optimizes the medical treatment of patients with ACS while providing an ideal infrastructure to evaluate and improve, both on a nation-wide and a single center scale, the adherence to guidelines. The median delay between symptom onset and first medical contact remains high. Although performed relatively rarely, a pre-hospital ECG facilitates earlier diagnosis of a STEMI in a large majority of patients. The introduction of CPUs minimizes in-hospital delays and exploits the benefit of invasive diagnostics and treatment.

Objective: Cardiac surgery on cardiopulmonary bypass (CPB) results in progressive myocardial dysfunction, despite unimpaired coronary blood flow, and is associated with increased myocardial tumor necrosis factor-alpha (TNF alpha) expression. We investigated whether anti-inflammatory treatment prevents increased TNF alpha expression and myocardial dysfunction after CPB. Methods and results: Baseline systemic hemodynamics, myocardial contractile function, aortic and coronary blood flow were measured in anesthetized pigs. Then, placebo (PLA; saline; n = 7) or methylprednisolone (MP; 30 mg/kg; n = 6) was infused intravenously and CPB was instituted. Global ischemia was induced for 10 min by aortic cross-clamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h, and 8 h following termination of CPB. Systemic TNF alpha-plasma concentrations and left ventricular TNF alpha expression were analyzed. With unchanged coronary blood flow in both groups, a progressive toss of myocardial contractile function to 38 +/- 2% of baseline (p < 0.01) and cardiac index to 48 +/- 6% of baseline (p < 0.01) at 8 h after CPB in PLA was attenuated in MP (myocardial function: 72 +/- 3%, p < 0.01 vs PLA; cardiac index: 78 +/- 6%, p < 0.05 vs PLA). Systemic TNFa was increased at 8 h in PLA compared to MP (243 +/- 34 vs 90 +/- 34 pg/ml, p < 0.05). Myocardial TNF alpha was increased at 8 h after CPB compared to baseline and MP (p < 0.05). Myocardial TNF alpha immunostaining was more pronounced in PLA than in MP (p < 0.05), with TNF alpha-mRNA localization predominantly to cardiomyocytes. Conclusions: Methylprednisolone attenuates both systemic and myocardial TNF alpha increases and progressive myocardial dysfunction induced by cardiac surgery, suggesting a key rote for TNF alpha. (c) 2006 Elsevier B.V. All rights reserved.

Background: While dyspnea is a common symptom in patients admitted to Chest Pain Units (CPUs) little is known about the impact of dyspnea on their outcome. The purpose of this study was to evaluate the impact of dyspnea on the short-term outcome of CPU patients. Methods: We analyzed data from a total of 9169 patients admitted to one of the 38 participating CPUs in this registry between December 2008 and January 2013. Only patients who underwent coronary angiography for suspected ACS were included. 2601 patients (28.4%) presented with dyspnea. Results: Patients with dyspnea at admission were older and frequently had a wide range of comorbidities compared to patients without dyspnea. Heart failure symptoms in particular were more common in patients with dyspnea (21.0% vs. 5.3%, p < 0.05) at admission. Importantly, in patients presenting with dyspnea the 3 month mortality was fourfold higher compared to patients without dyspnea (8.6% vs. 2.1%, p < 0.05, OR death: 4.40 95% CI 3.14-6.03). Interestingly, the mortality estimated from the GRACE risk score was below the actual mortality assessed after the 3 month follow-up. After adjustment for the GRACE risk score or for heart failure, dyspnea remained highly predictive of death and myocardial infarction within 3 months (OR death adjusted for heart failure: 2.99 95% CI 1.99-4.47 and OR death adjusted for GRACE risk score: 3.37 95% CI 2.27-4.99). Conclusion: Dyspnea is a common symptom in CPU patients. Our data show that dyspnea is associated with a fourfold higher 3 month mortality which is underestimated by the established ACS risk scores. To improve their predictive value we therefore propose to add dyspnea as an item to common risk scores. (C) 2014 Elsevier Ireland Ltd. All rights reserved.