Impaired Diastolic Recovery after Acute Myocardial Infarction as a Predictor of Adverse Events

Abstract

BackgroundTo investigate the impact of left ventricular (LV) diastolic functional recovery on major adverse cardiac events (MACE) 6 months after acute myocardial infarction (AMI) in patients with preserved LV systolic function.MethodsA total 463 patients with preserved LV systolic function at 6 months after an AMI were divided into two groups based on the extent of diastolic recovery assessed by echocardiography: group I (n = 241) showed improving diastolic function and group II (n = 222) did not. MACE included death, recurrent myocardial infarction, and rehospitalization due to heart failure, and these events were compared with the patients' characteristics at baseline.ResultsCompared with group I, the patients in group II were older and had a higher prevalence of hypertension and diabetes. Blood levels of hemoglobin and triglyceride were lower in group II, whereas the levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and of high-sensitivity C-reactive protein were higher in this group than in group I. MACE were significantly more frequent in group II than in group I. Age, elevated NT-proBNP, and impaired diastolic recovery were significant independent predictors of MACE.ConclusionDespite improvement in LV systolic function, LV diastolic function had not improved in 222 patients (47.9%) by the 6-month follow-up after the index AMI, and impaired diastolic functional recovery was found to be an independent predictor of MACE. Evaluation of diastolic function would be a useful way to stratify risk in patients discharged after an index AMI.

Plasma YKL-40 Elevation on Admission and Follow-Up Is Associated with Diastolic Dysfunction and Mortality in Patients with Acute Myocardial Infarction

“…BNP have primarily been dedicated to the diagnosis, prognosis, and monitoring treatment of congestive heart failure and have also been pointed out to be increased in the setting of AMI [ 22 – 24 ]. BNP is released from heart in response to increased ventricular wall stress [ 25 ]. Elevated BNP after AMI identifies patients at risk of adverse left ventricular remodelling, chronic left ventricular dysfunction, and congestive heart failure [ 25 – 27 ].…”

“…BNP is released from heart in response to increased ventricular wall stress [ 25 ]. Elevated BNP after AMI identifies patients at risk of adverse left ventricular remodelling, chronic left ventricular dysfunction, and congestive heart failure [ 25 – 27 ]. It is well known that BNP levels are correlated with age, renal function, intracardiac pressures, and ejection fraction [ 25 ].…”

Echocardiographic diastolic function evolution in patients with an anterior Q‐wave myocardial infarction: insights from the REVE‐2 study

“…In HF-PEF patients, diastolic dysfunction (DD) has been described as a marker of impaired cardiac remodelling and has also been associated with HF-PEF onset and adverse prognosis. 3,4 Myocardial fibrosis has been identified as one of the major pathways leading to adverse remodelling and DD after acute MI. [5][6][7][8] In subjects undergoing cardiac resonance imaging (excluding those referred for severe valvulopathy, congenital heart disease, pericarditis, or pericardial disease), those with normal diastolic function exhibited no or minimal fibrosis.…”

Protective Mechanism of A20 Protein Overexpression in Acute Myocardial Infarction Rats

“…Acute myocardial infarction (AMI) refers to the sharp decrease or interruption of coronary artery blood supply, part of myocardium develops local acute necrosis due to severe and persistent ischaemia, thus, causing a series of symptoms and signs. Its main clinical manifestations include sudden chest pain, shortness of breath accompanied or not accompanied with haemodynamic disorder, arrhythmia, shock and heart failure (1,2). Acute myocardial infarction is one of the most serious disease types in coronary heart disease and its early fatality rate is very high.…”

“…L Li1,2 , Z Wu3 , E Li 2 , L Zhang2 , L Li 1 Investigar el mecanismo protector de la sobreexpresión de la proteína con dedos de zinc A20 en ratas con infarto agudo de miocardio(IAM). Métodos: Cuarenta y cinco ratas Sprague Dawley (SD) fueron divididas aleatoriamente en un grupo simulado, un grupo modelo, y un grupo de observación.…”