Assessment of left ventricle diastolic function in myocardial infarction patients treated with primary angioplasty.
BACKGROUND
More than 5% of patients over the age of 65 have been found to develop heart failure, and over half of them preserve normal left ventricular systolic function. In the last few years, diastolic heart failure has become a serious clinical and epidemiological problem.


METHODS
This prospective study was carried out on 99 patients. Patients were evaluated up to three months after primary percutaneous coronary intervention (PCI). Evaluation was performed three times: within the first 24 hours after primary PCI, on day seven after PCI and at three months after PCI. We analyzed the relationship between the severity of left ventricle diastolic dysfunction and atherosclerosis risk factors, infarction site, maximum levels of cardiac biomarkers such as troponin I, CPK and CK-MB, CRP protein levels, angioplasty effectiveness, reperfusion time, TIMI and TMPG grade.


RESULTS
Most patients with ST elevation myocardial infarction (STEMI) treated with primary PCI demonstrated left ventricle diastolic dysfunction on the first day of myocardial infarction. Levels of cardiac biomarkers were significantly higher in patients with restrictive filling pattern. The inflammatory response (CRP levels) was found to have an important role in the development of diastolic abnormalities. There was a close relationship between diastolic and systolic function. Average values of left ventricular ejection fraction in patients with restrictive filling pattern were significantly lower than in those with impaired relaxation (44.7 vs. 52.7%; p < 0.001) and normal filling (54.2%; p = 0.002).


CONCLUSIONS
More than half of patients with a first STEMI have left ventricle diastolic dysfunction within the first day after PCI, and these abnormalities are still present three months after PCI. Time and effectiveness of reperfusion, CRP level, troponin I, max, CPK max and CK-MB max levels as well as left ventricular ejection fraction have an important influence on the development of diastolic dysfunction. Infarct extension contributes significantly to the process.
Misztal
Marcin
M
Coronary Artery Disease Department, Institute of Cardiology, Jagiellonian University, Kraków, Poland. mamis@interia.pl
Stopyra
Katarzyna
K
Gackowski
Andrzej
A
Zmudka
Krzysztof
K
Piwowarska
Wiesława
W
D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood; D003971:Diastole; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D013318:Stroke Volume; D013997:Time Factors; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D016277:Ventricular Function, Left
D015415:Biomarkers; D018836:Inflammation Mediators; D019210:Troponin I; D002097:C-Reactive Protein; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form