title: Functional mechanisms of myocardial microcirculation in left ventricular hypertrophy: a hypothetical model of capillary remodeling post myocardial infarction.
abstract: OBJECTIVE
  Left ventricular (LV) remodeling after myocardial infarction (MI) is characterized by myocyte hypertrophy and a disproportional capillary growth. We developed a hypothetical model of capillary remodeling mechanisms based on quantitative data of microcirculation determined by magnetic resonance (MR) imaging techniques and histology.
  
  
  METHODS
  Perfusion and regional capillary blood volume (RBV) were quantified 8 and 16 weeks after MI (mean 27.0+/-2.9% of the left ventricle 16 weeks post MI) or sham operation in rats using MR imaging and were correlated with morphometric data.
  
  
  RESULTS
  Maximum perfusion (ml/(g min)) in the remote area decreased from 5.69+/-0.63 to 3.48+/-0.48 compared to sham animals (5.33+/-0.31, p</=0.01) and showed a close inverse relation to hypertrophy. In contrast, maximum RBV in the remote area was similar to that of sham animals (16.79+/-0.42% and 16.52+/-0.33%, respectively) and did not change over time. Thus, mean transit time (MTT) was longer in remote than in sham myocardium. Morphology revealed that hypertrophy was inversely related to capillary density which was associated with an increase in capillary cross-sections.
  
  
  CONCLUSIONS
  Perfusion data in synopsis with histological observations demonstrate that the functional capillary length increases during hypertrophy post MI which is consistent with the increase of the mean transit time. Despite a relative decrease in capillary density, RBV may be restored by an increase in the cross-sections. In the light of almost maximum oxygen extraction under normal conditions, this hypertrophy related remodeling may be deleterious for tissue supply.
authors.affiliation: Medizinische Klinik und Poliklinik I, Universität Würzburg, Josef-Schneider-Strasse 2, Würzburg, Germany. waller_c@medizin.uni-wuerzburg.de
authors.forename: Christiane
authors.initials: C
authors.lastname: Waller
authors.forename: Karl-Heinz
authors.initials: KH
authors.lastname: Hiller
authors.forename: Daniela
authors.initials: D
authors.lastname: Pfaff
authors.forename: Stefan
authors.initials: S
authors.lastname: Gattenlöhner
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Wolfgang R
authors.initials: WR
authors.lastname: Bauer
mesh_terms: D000818:Animals; D002196:Capillaries / Q000473:pathology / Q000503:physiopathology; D048429:Cell Size; D003326:Coronary Circulation; D004195:Disease Models, Animal; D005260:Female; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D019028:Magnetic Resonance Imaging, Cine; D008833:Microcirculation; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000473:pathology; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014655:Vascular Resistance; D020257:Ventricular Remodeling