Chronic left ventricular pressure overload in normal and diabetic hearts.

• Type: Summary of Presentation in an International Conference
• Date: 2006

Authors

Vasconcelos M (Author) Other; Falcão-Pires I (Author) FMUP; Gonçalves N (Author) FMUP; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: European Heart Journal

Pages: 475-476

World Congress of Cardiology

Barcelona, SPAIN, 02 a 06 de Setembro de 2006

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Resumo (PT): Chronic left ventricular pressure (LVP) overload is thought to act synergistically with diabetes mellitus (DM) in the promotion of cardiac disturbances that lead to heart failure progression. The aim of this study was to investigate the haemodynamic effects of chronic LVP overload (by supra-renal aortic banding - AB) in normal and diabetic hearts. Male Wistar rats were randomly divided in: (i) non-DM animals (SHAM; n=6); (ii) non-DM animals with AB (AB; n=6); (iii) DM animals (type 1 DM induced by streptozotocin; n=6); (iv) DM animals with AB (DMAB; n=6). After 7 weeks tip micromanometers were inserted into the RV and LV to obtain the following parameters: systolic pressure (SP), systolic pressure of an isovolumetric beat (SPiso), end-diastolic pressure (EDP), dP/dtmax, dP/dtmin and time constant of relaxation tau. Results are presented in table 1 as mean ± SEM (p<0.05: *vs SHAM, †vs AB, ‡ vs DM). In non-DM animals chronic LVP overload induced RV and LV hypercontractility, accompanied by faster LV, but slower RV relaxation rates. DM per se induced a selective slowing of RV relaxation and a slight impairment of RV and LV contractility, only detected in response to isovolumetric beats by a decreased SPiso. Chronic LVP overload of DM hearts further slowed down RV and LV relaxation rates and induced a smaller increase in contractility than in non-DM hearts. Furthermore, in response to isovolumetric beats, LV-EDP increased 2.0±0.2mmHg in non-DM and 3.9±0.7mmHg in DM hearts, indicating a bigger intolerance to acute afterload elevations in DM. Chronic LVP overload did not alter this response. Table 1 SHAM AB DM DMAB RV LV RV LV RV LV RV LV SP (mmHg) 20 93 25 127 19 90 18 125 ±0.8 ±0.4 ±1.4* ±3.9* ±1.0 ±3.0 ±1.0*†‡ ±8.9*‡ SPiso (mmHg) 51 198 60 244 43 169 52 225 ±2.6 ±11 ±5.2 ±11 ±3.3 ±12 ±2.8 ±17 dP/dtmax (mmHg/s) 987 4879 1320 7759 868 4843 786 5719 ±72 ±26 ±91* ±414* ±47 ±304 ±49*†‡ ±465† dP/dtmin (mmHg/s) -786 -3460 -1024 -4496 -596 -3142 -498 -3427 ±52 ±286 ±61* ±232* ±62 ±334 ±63*†‡ ±227† EDP (mmHg) 1.1 1.8 1.8 0.7 1.0 0.9 1.2 1.1 ±0.4 ±0.5 ±0.4 ±0.4 ±0.3 ±0.4 ±1.0 ±0.4 tau (ms) 12 20 15 1.7 16 20 18 24 ±0.8 ±0.1 ±1.1* ±0.7* ±1.8* ±2.0 ±1.9* ±1.6*† In conclusion, contrary to non-DM, in DM hearts chronic LVP overload impairs both RV and LV function and exacerbates the dysfunction induced by DM per se.

Language: English

Type (Professor's evaluation): Scientific

Notes: World Congress of Cardiology, published in journal, European Heart Journal. 2006; Vol.27(Suppl.1):475-476.