Dataset Information

Effect of long-term treatment with trandolapril on Hsp72 and Hsp73 induction of the failing heart following myocardial infarction.

ABSTRACT: 1. The effect of long-term treatment of rats with chronic heart failure (CHF) following acute myocardial infarction with trandolapril, an angiotensin I-converting enzyme (ACE) inhibitor, on heat shock-induced Hsp72 and Hsp73 production was examined. 2. Acute myocardial infarction was induced by coronary artery ligation (CAL). The animals with CAL showed symptoms of CHF at the 8th week after the operation. The hearts isolated from animals with CAL at the 2nd and 8th week after surgery were subjected to hyperthermia at 42 degrees C for 15 min followed by 6-h perfusion (hyperthermia/6-h perfusion). 3. In the hearts isolated from the animals at the 2nd week, an approximate 20% decline in the rate pressure product (RPP) was seen after hyperthermia/6-h perfusion, which was similar to that in non-operated controls. In contrast, a significant reduction in the RPP after hyperthermia/6-h perfusion was seen in the hearts of rats with CHF. These hearts did not increase Hsp72 and Hsp73 production after hyperthermia. The decline in RPP was associated with failure in the production of myocardial Hsp72 and Hsp73. 4. When rats with CAL were treated with 3 mg kg(-1) day(-1) trandolapril from the 2nd to 8th week after the operation, the decline in RPP of the failing heart after hyperthermia was similar to that of the sham-operated rats. The induction of myocardial Hsp72 and Hsp73 production of the coronary artery-ligated rats after hyperthermia was reversed by treatment with trandolapril. 5. These findings suggest that the preserved ability to induce Hsp72 and Hsp73 production in the heart with CAL by trandolapril treatment may be attributed to the increased tolerance against heat stress-induced deterioration of myocardial contractile function.

SUBMITTER: Tanonaka K

PROVIDER: S-EPMC1573024 | biostudies-other | 2001 Nov

REPOSITORIES: biostudies-other

ACCESS DATA

Similar Datasets

Project description:BackgroundAlthough silent myocardial infarction (SMI) accounts for about one-half of the total number of myocardial infarctions (MIs), the risk of heart failure (HF) among patients with SMI is not well established.ObjectivesThe purpose of this study was to examine the association of SMI and clinically manifested myocardial infarction (CMI) with HF, as compared with patients with no MI.MethodsThis analysis included 9,243 participants from the ARIC (Atherosclerosis Risk In Communities) study who were free of cardiovascular disease at baseline (ARIC visit 1: 1987 to 1989). SMI was defined as electrocardiographic evidence of MI without CMI after the baseline until ARIC visit 4 (1996 to 1998). HF events were ascertained starting from ARIC visit 4 until 2010 in individuals free of HF before that visit.ResultsBetween ARIC visits 1 and 4, 305 SMIs and 331 CMIs occurred. After ARIC visit 4 and during a median follow-up of 13.0 years, 976 HF events occurred. The incidence rate of HF was higher in both CMI and SMI participants than in those without MI (incidence rates per 1,000 person-years were 30.4, 16.2, and 7.8, respectively; p < 0.001). In a model adjusted for demographics and HF risk factors, both SMI (hazard ratio [HR]: 1.35; 95% confidence interval [CI]: 1.02 to 1.78) and CMI (HR: 2.85; 95% CI: 2.31 to 3.51) were associated with increased risk of HF compared with no MI. These associations were consistent in subgroups of participants stratified by several HF risk predictors. However, the risk of HF associated with SMI was stronger in those younger than the median age (53 years) (HR: 1.66; 95% CI: 1.00 to 2.75 vs. HR: 1.19; 95% CI: 0.85 to 1.66, respectively; overall interaction p by MI type <0.001).ConclusionsSMI is associated with an increased risk of HF. Future research is needed to examine the cost effectiveness of screening for SMI as part of HF risk assessment, and to identify preventive therapies to improve the risk of HF among patients with SMI.

Dataset Information

Effect of long-term treatment with trandolapril on Hsp72 and Hsp73 induction of the failing heart following myocardial infarction.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets