Distinct effects of 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 Journal of Heart Failure

Initial page: 104

ESC Annual Congress 2006

Helsínquia, Finlândia, 17 a 20 de Junho de 2006

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

CORDIS: Health sciences > Medical sciences > Medicine > Cardiology

Other information

Resumo (PT): Chronic left ventricular pressure (LVP) overload acts synergistically with diabetes mellitus (DM) in the promotion of cardiac disturbances that lead to heart failure progression. We investigated the haemodynamic effects of chronic LVP overload (by supra-renaJ aortic banding - AB) in normal and diabetic hearts. Male Wistar rats were randomly dividedin: (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/dtma, x, dP/dtmin and time constant of rela, xation tau. Results are presented in Table 1 as mean 4- SEM. In non-DM animals chronic LVP overload induced RV&LV hypercontractility, accompanied by faster LV, but slower RV relaxation rates. DM per se induced a selective slowing of RV rela, xation and a slight impairment of RV&LV contractility, only detected in response to isovolumetric beats by a decreased SPiso. Chronic LVP overload of DM hearts further slowed down RV&LV rela, xation rates and induced a smaller in- Table 1 SHAM AB DM DMAB RV LV RV LV RV LV RV LV SP 20 93 25 127 19 90 (mmHg) ±0.8 ±0.4 ±1.4" ±3.9* ±1.0 ±3.0 SPiso 51 198 60 244 43 169 (mmHg) ±2.6 ±11 ±5.2 ±11 ±3.3 ±12 dP/dtmax 987 4879 1320 7759 868 4843 (mmHg/s) ±72 ±26 ±91" ±414" ±47 ±304 dP/dtmin -786 -3460 -1024 -4496 -596 -3142 (mmHg/s) ±52 ±286 ±61" ±232* ±62 ±334 EDP 1.1 1.8 1.8 0.7 1.0 0.9 (mmHg) ±0.4 ±0.5 ±0.4 ±0.4 ±0.3 ±0.4 tau 12 20 15 17 16 21 (ms) ±0.8 ±1.0 ±1.1" ±0.7* ±1.8" ±2.0 p<0.05: *vs SHAM, *vs AB, $vs DM. 18 125 ±1.0 *~'* ±8.9** 52 225 ±2.8 ±17 52±2.87 5719 86±49.~'$ ±465 ~" -498 -3427 ±63.~'$ ±227 ~" 1.2 1.1 ±0.1 ±0.4 18 24 ±1.9" ±1.6 ** crease in contractility than in non-DM hearts. Furthermore, in response to isovolumetric beats, LV-EDP increased 2.0-t-0.2mmHg in non-DM and 3.9-t-0.7mmHg in DM hearts, indicating a bigger intolerance to acute a£terload elevations in DM. Chronic LVP overload did not alter this response. In conclusion, contrary to non-DM, in DM hearts chronic LVP overload impairs both RV&LV function and exacerbates the dysfunction induced by DM per se. The latter requires an acute a£terload elevation to be more readily detectable.

Language: English

Type (Professor's evaluation): Scientific

Notes: ESC Annual Congress 2006, published in journal, European Journal of Heart Failure. 2006; Vol.5(Suppl.1):104-104.