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LOW CORONARY DRIVING PRESSURE IS ASSOCIATED WITH SUBENDOCARDIAL REMODELLING AND LEFT VENTRICULAR DYSFUNCTION IN AORTOCAVAL FISTULA
Author(s) -
Guido Maria C,
De Carvalho Frimm Clovis,
Koike Márcia K,
Cordeiro Fernanda F,
Moretti Ana IS,
Godoy Luiz C
Publication year - 2007
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04689.x
Subject(s) - medicine , cardiology , endocardium , ventricle , hemodynamics , context (archaeology) , blood pressure , perfusion , left ventricular hypertrophy , myocardial fibrosis , fibrosis , ventricular remodeling , ventricular pressure , coronary perfusion pressure , coronary circulation , myocardial infarction , surgery , blood flow , resuscitation , cardiopulmonary resuscitation , paleontology , biology
SUMMARY1 The role of haemodynamic changes in left ventricular remodelling has been poorly investigated, especially in the context of volume overload cardiac hypertrophy. Low diastolic blood pressure and high left ventricular filling pressure are expected to affect coronary driving pressure negatively and thereby put in jeopardy subendocardial perfusion in particular. The consequences to global left ventricular remodelling remain undetermined. The aim of the present study was to investigate the role of coronary driving pressure in the development of subendocardial remodelling and the conceivable effects on cardiac function, using a rat model of aortocaval fistula. 2 Wistar rats, weighing 330–350 g, were submitted to aortocaval fistula (ACF group) or sham (control group) operations. Two haemodynamic measurements were determined following surgery, the initial measurement at week 1 and the final measurement at week 8. Cytokine expression, myeloperoxidase (MPO) activity, metalloproteinase expression and activity and fibrosis were assessed in two distinct left ventricular myocardial layers: the subendocardium (SE) and the non‐subendocardium (non‐SE). 3 The ACF group showed lower initial and final coronary driving pressure and lower final +dP/dt and –dP/dt compared with the control group. Multivariate analyses disclosed initial coronary driving pressure as the only haemodynamic parameter independently associated with SE fibrosis ( R 2 = 0.76; P < 0.0001) and with +dP/dt ( R 2 = 0.55; P = 0.0004) and –dP/dt ( R 2 = 0.91; P < 0.0001). Matrix metalloproteinase (MMP)‐2 expression and activity predominated in the SE of ACF animals, particularly in those with low coronary driving pressure. Increased levels of interleukin (IL)‐6 and IL‐1β also predominated in the SE of the ACF group. Otherwise, MPO activity and levels of tumour necrosis factor‐α and IL‐10 were similar in both groups. Final coronary driving pressure correlated with both the expression and activity of MMP‐2. 4 Low coronary driving pressure early in the course of ACF determines SE damage and, by this mechanism, interferes negatively in left ventricular function.