Impact of chronotropic effect of cilostazol after acute myocardial infarction: insights from change in left ventricular volume and function.
Cardiology Division, Kangnam Sacred Heart Hospital, Hallym University College of Medicine, Seoul, Republic of Korea. Circulation Journal
(Impact Factor: 3.94).
Cilostazol, a phosphodiesterase inhibitor, is an antiplatelet agent with positive chronotropic effect, the impact of which on left ventricular (LV) volume and function in acute myocardial infarction (AMI) was evaluated in the present study.
In 56 patients with AMI treated with primary coronary stenting, serial echocardiographic studies within 24 h and at 6 months were performed. Patients received a conventional antiplatelet regimen either without cilostazol (group 1, n=29) or with cilostazol (group 2, n=27). At 6 months, the difference in the change in heart rate between group 1 and group 2 was statistically significant (9.9 beats/min; p=0.04). However, changes in LV end-systolic volume (LVESV) (7.1+/-8.2 vs 10.0+/-21.7 ml, p=0.60), LV ejection fraction (EF) (8.2+/-9.9 vs 9.0+/-12.6%, p=0.85) and the ratio of early mitral inflow velocity to the mitral annular velocity (E/E') (0.6+/-3.7 vs -1.7+/-3.2) were not different between the 2 groups. Cardiac event rate was similar between the 2 groups. On multivariate regression analyses, cilostazol therapy had no significant influence on the changes in LVESV, LVEF or E/E'.
In this study, the addition of cilostazol on conventional drug therapy had no adverse influence on LV remodeling or LV function after AMI.
Available from: Byung-Hee Oh
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ABSTRACT: Positive longitudinal pre-ejectional velocity (+PEVL) was recently reported to be a reliable index of myocardial recovery early after successful revascularization in myocardial infarction (MI); that is, it recognizes the transmural extent of viable myocardium. The applicability of PEVL in the real-world clinical setting for identifying the transmural extent of viable myocardium in reperfused recent MI was assessed.
Using tissue Doppler imaging, the resting basal and mid myocardial PEVLs were determined within 3 days after revascularization in 41 consecutive patients with recent MI. Infarct thickness was semi-quantified using delayed gadolinium-enhanced magnetic resonance imaging (MRI) at baseline and at 6-month follow up to differentiate transmural from nontransmural MI. The proportion of segments showing the presence of +PEVL was not significantly changed as infarct thickness increased (p=0.2), with 66.2% having +PEVL even in segments involving >75% transmural infarction. Moreover, +PEVL was found in a large fraction of segments with akinesia (70.4%). Specificity and negative predictive value of +PEVL for assessing infarct nontransmurality were disappointingly low (32.0% and 26.9%, respectively). All of these results were not altered when the 6-month follow-up MRI was done.
+PEVL cannot be regarded as a reliable marker for predicting the transmural extent of viable myocardium in recent MI.
Circulation Journal 12/2007; 71(12):1904-11. · 3.94 Impact Factor
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ABSTRACT: This study was designed to investigate the efficacy of cilostazol on the prevention of in-stent neointimal hyperplasia as measured by both quantitative coronary angiography (CAG) and volumetric intravascular ultrasound (IVUS).
Fifty-nine patients (39 men, age 62 years) undergoing elective coronary stenting were randomly assigned to receive aspirin plus clopidogrel or ticlopidine (Group I, n=28, 30 lesions) or aspirin plus clopidogrel or ticlopidine plus cilostazol (Group II, n=31, 35 lesions). CAG and IVUS were performed and repeated at 6 months to assess the primary endpoints of minimal luminal diameter (MLD) and in-stent neointimal hyperplasia volume. Follow-up CAG was performed on all patients and follow-up IVUS study was available for 50 lesions in 48 patients (24 lesions in Group I, 26 in Group II). There were no significant differences in the baseline angiographic data between the 2 groups. At 6 months follow-up, in-stent MLD was 1.90+/-0.76 mm in Group I and 2.41+/-0.85 mm in Group II (p=0.006). Volumetric IVUS at 6 months demonstrated that in-stent intimal hyperplasia volume per stent length was 2.2+/-1.4 mm3/mm in Group I and 1.0+/-0.5 mm3/mm in Group II (p=0.001).
Triple antiplatelet therapy including cilostazol seems to be more effective at preventing in-stent neointimal hyperplasia than a dual antiplatelet regimen.
Circulation Journal 12/2007; 71(11):1685-90. · 3.94 Impact Factor
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ABSTRACT: Cilostazol, a type III phosphodiesterase inhibitor, is an antiplatelet agent with vasodilating properties. Positive inotropic and chronotropic effects are frequently observed with cilostazol, but there are few reports on the influence of cilostazol on left ventricular function. The aim of this study was to assess this effect using tissue Doppler imaging (TDI) and two-dimensional speckle-tracking echocardiography (2D-STE).
Thirty-five patients with normal left ventricular ejection fraction were enrolled in the study. Left ventricular cardiac function was assessed by TDI and 2D-STE before and after oral administration of cilostazol. Peak strain was defined using the peak radial strain (PRS), peak circumferential strain (PCS) and peak longitudinal strain (PLS). Time to peak strain was defined based on the times to PRS, PCS, and PLS, as T-PRS, T-PCS, and T-PLS, respectively.
After cilostazol administration, there were significant decreases in the left ventricular end-diastolic and end-systolic diameters (47.3 ± 5.2 vs. 43.3 ± 4.9 mm, P < 0.0001; 29.3 ± 6.4 vs. 26.0 ± 5.5 mm, P < 0.0001, respectively), and significant increases in the left ventricular ejection fraction (70.6 ± 9.5 vs. 72.7 ± 7.8%, P = 0.0381) and peak systolic annular velocity (7.9 ± 1.7 vs. 9.5 ± 3.1 cm/sec, P < 0.0001). PRS, PCS, and PLS all increased significantly and T-PRS, T-PCS, and T-PLS all decreased significantly after cilostazol administration.
Positive inotropic and chronotropic effects of cilostazol were found based on assessment by TDI and 2D-STE. We suggest that periodic echocardiographic assessment should be performed before and after oral administration of cilostazol.
Echocardiography 04/2011; 28(4):431-7. DOI:10.1111/j.1540-8175.2010.01357.x · 1.25 Impact Factor
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