Paul M. Haller works in Interventional Cardiology affiliated with Universität Hamburg.
Paul M. Haller is an assistant physician in the Department of Cardiology at the University Heart & Vascular Center Hamburg in Germany. He serves as a research fellow at the TIMI Study Group in the Division of Cardiovascular Medicine at Brigham and Women's Hospital and Harvard Medical School. His work includes research on acute myocardial infarction, cardiac imaging, and heart failure.
139 pubs · 1,633 cites · h-index 20
Research Fellow
TIMI Study Group, Brigham and Women's Hospital, Harvard Medical School · 2023 - Present
Assistant Physician
University Heart & Vascular Center Hamburg
Affiliated Researcher, Division of Cardiology
Medical University of Vienna
Standard modifiable risk factors are present in over 99% of patients ultimately diagnosed with acute MI, and their absence allows the ESC 0/1-hour hs-cTnI algorithm to rule out MI in 72.1% of SMuRF-less patients with a 100% negative predictive value.
Elevated hs-CRP may enhance long-term risk stratification beyond GRACE in observe-zone patients; hypothesis-generating and requires prospective validation before adoption.
HF polygenic risk score was associated with incident heart failure; leaves open whether it improves clinical risk stratification or prevention.
Research fellow, TIMI Study Group, Brigham and Women's · Brigham and Women's Hospital
The important finding this paper suggests is that a dual-marker strategy that includes both of these biomarkers could be of greater value for predicting heart-failure events in patients with atrial fibrillation than only considering NTproBNP.
Journal of the American College of CardiologyHaller et al.
Early and sustained treatment with evolocumab significantly reduces the need for complex coronary revascularization compared to delayed initiation.
Myocardial injury in hypertensive crisis signals higher 2-year mortality; hypothesis-generating for etiology-specific risk stratification.
3h rule-out warrants closer surveillance; challenges prognostic equivalence of delayed versus 0/1h hs-cTnT triage.
Analysis shows multiple imputation and bivariate meta-analysis can enhance precision in cardiovascular trials, retaining valuable information.
Analysis reveals galectin-3 levels correlate with kidney disease risk in type 2 diabetes patients, suggesting dapagliflozin may reduce risk of kidney-related outcomes.
In-hospital initiation of dapagliflozin did not significantly reduce the primary composite of cardiovascular death or worsening heart failure at two months, though a prespecified meta-analysis suggests SGLT2 inhibitors as a class may reduce early risk in this setting.
May support outpatient work-up in low-risk observe-zone NSTE-ACS; leaves open need for prospective validation.
The 3C algorithm offers a uniform, assay-agnostic alternative to established ESC algorithms for diagnosing MI, with comparable diagnostic accuracy.
Propensity-matched cohort study demonstrates pre-hospital heparin does not improve survival in suspected acute coronary syndrome, suggesting restricting use until in-hospital risk evaluation.
No significant stroke or embolism difference with DOACs; leaves open optimal anticoagulation strategy and requires randomized confirmation.
May aid risk stratification in suspected MI; hypothesis-generating and requires prospective validation before practice change.
Myocardial injury signals high all-cause mortality risk; hypothesis-generating for targeted interventions in prospective studies.
Sex-specific hs-cTn thresholds do not improve MI diagnosis over unisex cutoffs; leaves open any added prognostic value in observational cohorts.
Background and aims: It is suggested that the changes in atherosclerosis happen mainly under the influence of non-fasting lipids. To date, the studies in the postprandial state were primarily performed on healthy subjects. This exploratory, cross-sectional study investigates the change in lipid profile, inflammation, and platelet activation in patients with different cardiovascular risk profiles in the postprandial state. Methods: The studied population consists of 66 patients with different cardiovascular risks: patients with a history of the chronic coronary syndrome (CCS) and diabetes mellitus type 2 (DM2) (n = 20), CCS without DM2 (n = 25), and a healthy control group (n = 21). Lipid variables and markers of platelet function and inflammation were assessed during the fasting state and three and 5 h after a standardized fat meal using a standardized oral fat tolerance test (OFTT), a milkshake with 90 g of fat. Results: Patients with CCS and DM2 were significantly older and had the highest BMI. All patients with CCS were on acetylsalicylic acid, and 95% of CCS patients were on high-dose statins. The absolute leukocyte and neutrophile count increased significantly in the control group during the OFTT in comparison to CCS subjects. There was a significant decrease of HDL and increase of triglycerides during the OFTT, however with no difference between groups. There was no difference in the change of platelet activity between all groups. Conclusion: This study showed that OFTT leads to an increased postprandial inflammation response in healthy group compared to CCS ± DM2 while there was no change in lipid profile and platelet activity.
