Effects of Verapamil Cardioplegia on the Hypertrophied Left Ventricle Undergoing Cardiopulmonary Bypass.
10.4097/kjae.2000.39.6.804
- Author:
Won Sun PARK
1
;
Young Lan KWAK
;
Chun Soo LEE
;
Jin Ho KIM
;
Won Cheol KANG
;
Yong Woo HONG
Author Information
1. Department of Anesthesiology, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article ; Randomized Controlled Trial
- Keywords:
Heart: myocardial protection;
ventricular hypertrophy;
verapamil cardioplegia;
Monitoring: transesophageal echocardiography;
Surgery: cardiac
- MeSH:
Calcium Channels;
Cardioplegic Solutions;
Cardiopulmonary Bypass*;
Edema;
Heart;
Heart Arrest, Induced*;
Heart Ventricles*;
Hemodynamics;
Humans;
Ischemia;
Myocardium;
Reperfusion Injury;
Stroke Volume;
Verapamil*
- From:Korean Journal of Anesthesiology
2000;39(6):804-810
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Verapamil, a calcium channel blocker, is known to protect the myocardium against ischemia and reperfusion injury. The hypertrophied myocardium is at greater risk for ischemic damage compared to the normal heart during cardiopulmonary bypass (CPB). We evaluated the myocardial protective effect of verapamil cardioplegia on the hypertrophied left ventricle during CPB. METHODS: Seventeen patients with end-diastolic anterior wall thickness (DAWT) greater than 11 mm in an M-mode echocardiogram were consented to participate in this study. Patients were randomized to receive either standard hyperkalemic blood cardioplegic solution (n = 8) or the same solution with verapamil (n = 9). End systolic anterior wall thickeness (SAWT) and DAWT were measured by an M-mode echocardiogram and the left ventricular ejection fraction (LVEF) was calculated with a 2-dimension echocardiogram before and after CPB. Simultaneously, hemodynamic variables were measured. RESULTS: There was no significant difference of DAWT and LVEF between both groups before and after CPB. DAWT was increased after CPB but this increase was attenuated by verapamil in patients with LVH. LVEF was decreased in both groups after CPB and the decrease in the verapamil group was not statistically significant but in the control group. Cardiac index and stroke volume index didn't show any significant differences between the two groups after CPB, either. CONCLUSIONS: DAWT increased which means myocardial edema was significant in patients with LVH; however, a verapamil cardioplegic solution decreased the amount of increase in DAWT. However, theverapamil cardioplegic solution didn't improve the hypertophied ventricular systolic function after CPB.
