title: Effect of diltiazem on cardiac function assessed by echocardiography and neurohumoral factors after reperfused myocardial infarction without congestive heart failure.
abstract: The purpose of this study was to examine the effect of diltiazem on cardiac function and neurohumoral factors (BNP, epinephrine, norepinephrine) after reperfused myocardial infarction without congestive heart failure (Killip class I). On the first day after myocardial infarction following reperfusion therapy patients were randomly assigned to diltiazem treatment (group 1, n=33) or no treatment (group 2, n=39). We then performed echocardiographic examinations on the patients and measured heart rate, mean blood pressure and neurohormones (BNP, epinephrine and norepinephrine). Follow-up evaluations of echocardiography were performed at 4 and 12 weeks and of neurohormones at 1 and 4 weeks after acute myocardial infarction. The highest peaks of plasma BNP, epinephrine, and norepinephrine levels were observed before treatment and decreased with time in both groups. After 4 weeks the level of plasma BNP in the diltiazem treatment group was lower than in the no treatment group [55+/-3 pg/mL vs 85+/-5 pg/mL (P < 0.05)]. Other neurohormones did not differ between groups. Fractional shortening (FS) and ejection fraction (EF)improved after myocardial infarction in both groups, but significantly more in the diltiazem group (P < 0.05) after 12 weeks of treatment. Changes in BNP correlated significantly with changes in left ventricular end systolic volumes, FS and EF. In this study, diltiazem significantly improved systolic function and reduced the level of plasma BNP after myocardial infarction, which suggest that diltiazem may have a beneficial effect on myocardial infarction without congestive heart failure.
authors.affiliation: Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Maki
authors.forename: M
authors.initials: M
authors.lastname: Yoshiyama
authors.forename: T
authors.initials: T
authors.lastname: Omura
authors.forename: T
authors.initials: T
authors.lastname: Yoshimura
authors.forename: T
authors.initials: T
authors.lastname: Kawarabayashi
authors.forename: K
authors.initials: K
authors.lastname: Sakamoto
authors.forename: K
authors.initials: K
authors.lastname: Hirota
authors.forename: H
authors.initials: H
authors.lastname: Iida
authors.forename: K
authors.initials: K
authors.lastname: Takeuchi
authors.forename: J
authors.initials: J
authors.lastname: Yoshikawa
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000187:drug effects; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D004110:Diltiazem / Q000627:therapeutic use*; D004452:Echocardiography; D004837:Epinephrine / Q000097:blood; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006333:Heart Failure / Q000517:prevention & control; D006334:Heart Function Tests; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D018377:Neurotransmitter Agents / Q000097:blood*; D009638:Norepinephrine / Q000097:blood; D011446:Prospective Studies; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D002317:Cardiovascular Agents; D018377:Neurotransmitter Agents; D020097:Natriuretic Peptide, Brain; D004110:Diltiazem; D009638:Norepinephrine; D004837:Epinephrine