Neurohormonal changes after acute myocardial infarction

Foy, S. G.; Crozier, Ian; Richards, A. Mark; Nicholls, M. Gary; Turner, J. G.; Frampton, Christopher M.; Ikram, Hamid

doi:10.1093/oxfordjournals.eurheartj.a060995

Cited by 47 publications

(7 citation statements)

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“…Thus, IR injury may have accelerated or enhanced the effects of diabetes on accumulation of collagen in the heart. It is well known that the hemodynamic and neurohormonal changes in the period after MI stimulate events such as intense activation of both the circulating and the local renin-angiotensin-aldosterone system [43]. It has also been reported that diabetes is coupled with an activation of the renin-angiotensin system in the heart [44].…”

Section: Discussionmentioning

confidence: 99%

Ischemia-Reperfusion Injury Leads to Distinct Temporal Cardiac Remodeling in Normal versus Diabetic Mice

et al. 2012

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Diabetes is associated with higher incidence of myocardial infarction (MI) and increased propensity for subsequent events post-MI. Here we conducted a temporal analysis of the influence of diabetes on cardiac dysfunction and remodeling after ischemia reperfusion (IR) injury in mice. Diabetes was induced using streptozotocin and IR performed by ligating the left anterior descending coronary artery for 30 min followed by reperfusion for up to 42 days. We first evaluated changes in cardiac function using echocardiography after 24 hours reperfusion and observed IR injury significantly decreased the systolic function, such as ejection fraction, fractional shortening and end systolic left ventricular volume (LVESV) in both control and diabetic mice. The longitudinal systolic and diastolic strain rate were altered after IR, but there were no significant differences between diabetic mice and controls. However, a reduced ability to metabolize glucose was observed in the diabetic animals as determined by PET-CT scanning using 2-deoxy-2-(18F)fluoro-D-glucose. Interestingly, after 24 hours reperfusion diabetic mice showed a reduced infarct size and less apoptosis indicated by TUNEL analysis in heart sections. This may be explained by increased levels of autophagy detected in diabetic mice hearts. Similar increases in IR-induced macrophage infiltration detected by CD68 staining indicated no change in inflammation between control and diabetic mice. Over time, control mice subjected to IR developed mild left ventricular dilation whereas diabetic mice exhibited a decrease in both end diastolic left ventricular volume and LVESV with a decreased intraventricular space and thicker left ventricular wall, indicating concentric hypertrophy. This was associated with marked increases in fibrosis, indicted by Masson trichrome staining, of heart sections in diabetic IR group. In summary, we demonstrate that diabetes principally influences distinct IR-induced chronic changes in cardiac function and remodeling, while a smaller infarct size and elevated levels of autophagy with similar cardiac function are observed in acute phase.

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Section: Discussionmentioning

confidence: 99%

Ischemia-Reperfusion Injury Leads to Distinct Temporal Cardiac Remodeling in Normal versus Diabetic Mice

et al. 2012

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“…The majority of information on autonomic function post‐MI has been derived from the use of indirect indices. In earlier studies, venous catecholamines were measured sequentially post‐MI, and a minor immediate increase was demonstrated which normalized within 12 h unless heart failure supervened (Karlsberg et al 1981; McAlpine et al 1988; Sigurdsson et al 1993; Foy et al 1995). The contribution of the heart, versus other tissues and organs, to this increase in venous catecholamine levels remains uncertain and, given that plasma levels may be affected by regional variations in their release and by changes in their clearance rate, plasma catecholamines are a crude estimate of sympathetic output (Esler et al 1990).…”

Section: Discussionmentioning

confidence: 99%

Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model

Jardine

Charles²,

Ashton³

et al. 2005

The Journal of Physiology

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The time course of cardiac sympathetic nerve activity (CSNA) following acute myocardial infarction (MI) is unknown. We therefore undertook serial direct recordings of CSNA, arterial blood pressure (MAP) and heart rate (HR) in 11 conscious sheep before and after MI, and compared them with 10 controls. Conscious CSNA recordings were taken daily from electrodes glued into the thoracic cardiac nerves. Infarction was induced under pethidine and diazepam analgesia by applying tension to a coronary suture. MI size was assessed by left ventricular planimetry (%) at postmortem, peak troponin T and brain natriuretic peptide levels (BNP). Baroreflex slopes were assessed daily using phenylephrine-nitroprusside ramps. The mean infarcted area was 14.4 ± 2.9%, troponin T 1.88 ± 0.39 µg l −1 and BNP 8.4 ± 1.3 pmol l −1 . There were no differences in haemodynamic parameters or CSNA between groups at baseline. MAP and HR remained constant following MI. CSNA burst frequency increased from baseline levels of 55.8 ± 7.1 bursts min −1 to levels of 77.5 ± 8.7 bursts min −1 at 2 h post-MI, and remained elevated for 2 days (P < 0.001). CSNA burst area also increased and was sustained for 7 days following MI (P = 0.016). Baroreflex slopes for pulse interval and CSNA did not change. CSNA increases within 1 h of the onset of MI and is sustained for at least 7 days. The duration of this response may be longer because the recording fields decrease with time. This result is consistent with a sustained cardiac excitatory sympathetic reflex.

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“…AMI is associated with a complex pattern of neurohumoral activation in which catecholamines play an important role in both onset and course of AMI [ 4 , 5 ]. Catestatin is a 21-amino acid residue, cationic and hydrophobic peptide which is generated endogenously by proteolytic cleavage of its precursor chromogranin A (CHGA) [ 6 ], a protein found in secretory granules of chromaffin cells, postganglionic sympathetic neurons [ 7 ] and heart cells itself [ 8 ], where it was co-stored and co-released with catecholamines.…”

Section: Introductionmentioning

confidence: 99%

Correlation of Plasma Catestatin Level and the Prognosis of Patients with Acute Myocardial Infarction

et al. 2015

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Catestatin is a peptide which is a potent inhibitor of catecholamine secretion and played essential functions in the cardiovascular system. Previous research found that dramatic changes of catestatin were associated with hemodynamics in acute myocardial infarction (AMI) during the first week after the AMI symptoms onset, but whether catestatin is also involved in the pathophysiological progression after AMI and then a predictor for outcomes is not clear. The aim of this study is to determine the correlation of plasma catestatin levels at different time points and the prognosis of AMI. 100 participants recruited were all patients with AMI, all of who received successful primary percutaneous coronary intervention (PCI) within 12h from the AMI symptom onset in our center; the concentrations of plasma catestatin were evaluated from blood samples of those 100 participants. Subsequent 65 months' follow-up was performed after discharging to evaluate cardiac adverse events and the association between catestatin levels and prognosis of AMI was examined. We confirmed the dramatic change of catestatin concentrations in the first week of AMI, and the levels of catestatin on D3 were much higher in adverse events group than those in non-adverse events group (p<0.0001), but the ratio of D7/D3 was significantly lower. In addition, the Kaplan-Meier analysis showed that the groups in which the levels on D3 were higher (p<0.0001) and the ratios of D7/D3 were lower (p<0.0001), patients trended to be more susceptive to adverse events after AMI. Furthermore, according to the analysis, we surmised catestatin level on D3 as an appropriate predictor for outcomes in patients with AMI with good specificity as well as sensitivity. All of the evidence confirmed that catestatin plays an important role in the progress of AMI, and may act as a promising target for prognostic prediction.

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Neurohormonal changes after acute myocardial infarction

Cited by 47 publications

References 0 publications

Ischemia-Reperfusion Injury Leads to Distinct Temporal Cardiac Remodeling in Normal versus Diabetic Mice

Ischemia-Reperfusion Injury Leads to Distinct Temporal Cardiac Remodeling in Normal versus Diabetic Mice

Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model

Correlation of Plasma Catestatin Level and the Prognosis of Patients with Acute Myocardial Infarction

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