M
Marcel J.M. Kofflard
Researcher at Albert Schweitzer Hospital
Publications - 78
Citations - 2176
Marcel J.M. Kofflard is an academic researcher from Albert Schweitzer Hospital. The author has contributed to research in topics: Hypertrophic cardiomyopathy & Cardiomyopathy. The author has an hindex of 21, co-authored 73 publications receiving 1934 citations. Previous affiliations of Marcel J.M. Kofflard include Erasmus University Rotterdam.
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Journal ArticleDOI
Hypertrophic cardiomyopathy in a large community-based population: clinical outcome and identification of risk factors for sudden cardiac death and clinical deterioration
TL;DR: Syncope was associated with a higher incidence of SCD and patients with a significant LVOT obstruction were more susceptible to clinical deterioration and Hypertrophic cardiomyopathy is a benign disease in an unselected population with a low incidence of cardiac death.
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Decreased Coronary Flow Reserve in Hypertrophic Cardiomyopathy Is Related to Remodeling of the Coronary Microcirculation
Rob Krams,Marcel J.M. Kofflard,Dirk J. Duncker,C. von Birgelen,Stephane Carlier,Mike Kliffen,F. J. Ten Cate,P. W. Serruys +7 more
TL;DR: Both the decrease in CRR and these changes in the coronary microcirculation were related to the degree of hypertrophy, and these factors might contribute to the well-known occurrence of ischemia in this patient group.
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Late lumen loss after coronary angioplasty is associated with the activation status of circulating phagocytes before treatment
Anneke Pietersma,Marcel J.M. Kofflard,L. Elly A. de Wit,Theo Stijnen,Johan F. Koster,Patrick W. Serruys,Wim Sluiter +6 more
TL;DR: It is found that activated blood granulocytes prevent luminal renarrowing after PTCA, while activated blood monocytes promote late lumen loss.
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Association of plasma fibrinogen levels with coronary artery disease, smoking and inflammatory markers
TL;DR: The results indicate that both smoking and CAD induce an inflammatory condition but that the increase of plasma levels of different inflammatory markers is complex, although the acute phase reaction is the main regulatory mechanism of fibrinogen.
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AT1 Receptor A/C1166 Polymorphism Contributes to Cardiac Hypertrophy in Subjects With Hypertrophic Cardiomyopathy
Arthur P. R. M. Osterop,Marcel J.M. Kofflard,Lodewijk A. Sandkuijl,Folkert J. ten Cate,Rob Krams,Maarten A.D.H. Schalekamp,A.H. Jan Danser +6 more
TL;DR: It is concluded that the AT1-R C1166 allele modulates the phenotypic expression of hypertrophy in HCM, independently of plasma renin and the ACE I/D polymorphism.