
Preinfarction angina prevents left ventricular remodeling in patients treated with thrombolysis for myocardial infarction
Author(s) -
NeŠKOVIÉ Aleksandar N.,
Pavlovski KoČO,
Bojić Dragana,
Popović Zoran,
Ota ević Petar,
Vlahovićca Alja,
Obradovićca Velibor,
Putnikovićca Biljana,
VasiljevićcaPokraj Zorana,
Bojićca Milovan,
Popovićca Aleksandar D.
Publication year - 2001
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960240504
Subject(s) - medicine , cardiology , angina , myocardial infarction , ejection fraction , ventricular remodeling , infarction , thrombolysis , heart failure
Background: It has been shown that preinfarction angina may have beneficial effects on infarct size and mortality. However, there are no studies that have serially assessed the impact of preinfarction angina on left ventricular (LV) function in a large series of patients. Hypothesis: The study was undertaken to determine whether preinfarction angina (within 7 days before infarction) influences LV remodeling. Methods: In all, 119 consecutive patients with acute myocardial infarction were serially evaluated by 2‐dimensional echocardiography (on Days 1, 2, 3, and 7; at 3 and 6 weeks; and at 3, 6, and 12 months following infarction). Left ventricular volumes were determined using Simpson's biplane formula and normalized for body surface area. Wall motion score index and sphericity index were calculated for each study. Coronary angiography was performed before discharge. Results: Preinfarction angina was detected in 39 of 119 patients. Initial echocardiographic and clinical data as well as the incidence of patent infarct‐related artery and collaterals were similar for patients with and without preinfarction angina. In the subset of thrombolysed patients, patients with preinfarction angina showed decrease of LV end‐diastolic and end‐systolic volumes during the follow‐up period (p = 0.033 and p = 0.001, respectively), and improvement of wall motion score index (p < 0.001) and ejection fraction occurred (p = 0.001), without changing of LV shape (p > 0.05); in addition, patients with preinfarction angina had smaller LV volumes and higher ejection fraction than did those without angina, from 3 weeks onward. These favorable effects were not detected in patients not treated with thrombolysis. Conclusions: These data indicate that preinfarction angina has an inhibiting effect on long‐term LV remodeling in patients who underwent thrombolysis for first acute myocardial infarction. It appears that preinfarction angina has no impact on infarct size and early postinfarction LV function.