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      Different Effects of Calcium Antagonist and Beta-Blocker Therapy on Left-Ventricular Diastolic Function in Ischemic Heart Disease


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          Objective: To compare the effect of a calcium antagonist and a beta-blocker on left-ventricular diastolic function in patients with ischemic heart disease. Methods: 138 patients with chronic stable angina pectoris were randomized in a multicenter, double-blind trial to treatment with either mibefradil or atenolol for 6 weeks (50 mg once daily for 2 weeks followed by 100 mg once daily for 4 weeks). The ratio between early (E) and late (A) diastolic mitral flow velocities (E/A), the E wave deceleration time (DT) and the left ventricular isovolumetric relaxation time (IRT) were measured by Doppler echocardiography as parameters of left-ventricular diastolic function initially, after 4 and after 6 weeks of treatment. Results: Mibefradil did not change the E/A ratio significantly (+4%, NS), while atenolol treatment resulted in a significant increase in the E/A ratio (+20%, p < 0.001). Mibefradil treatment, on the other hand, resulted in a significant decrease (–8%, p < 0.001) in IRT, while atenolol treatment did not change IRT. Neither mibefradil nor atenolol treatment changed DT significantly. Conclusions: Both mibefradil and atenolol treatment significantly improves echocardiographic indices of left-ventricular diastolic function in patients with chronic stable angina. However, they affect different parameters and thus apparently act through different mechanisms.

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          A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group.

          Treatment with angiotensin-converting-enzyme (ACE) inhibitors reduces mortality among survivors of acute myocardial infarction, but whether to use ACE inhibitors in all patients or only in selected patients is uncertain. We screened 6676 consecutive patients with 7001 myocardial infarctions confirmed by enzyme studies. A total of 2606 patients had echocardiographic evidence of left ventricular systolic dysfunction (ejection fraction, < or = 35 percent). On days 3 to 7 after infarction, 1749 patients were randomly assigned to receive oral trandolapril (876 patients) or placebo (873 patients). The duration of follow-up was 24 to 50 months. During the study period, 304 patients (34.7 percent) in the trandolapril group died, as compared with 369 (42.3 percent) in the placebo group (P = 0.001). The relative risk of death in the trandolapril group, as compared with the placebo group, was 0.78 (95 percent confidence interval, 0.67 to 0.91). Trandolapril also reduced the risk of death from cardiovascular causes (relative risk, 0.75; 95 percent confidence interval, 0.63 to 0.89; P = 0.001) and sudden death (relative risk, 0.76; 95 percent confidence interval, 0.59 to 0.98; P = 0.03). Progression to severe heart failure was less frequent in the trandolapril group (relative risk, 0.71; 95 percent confidence interval, 0.56 to 0.89; P = 0.003). In contrast, the risk of recurrent myocardial infarction (fatal or nonfatal) was not significantly reduced (relative risk, 0.86; 95 percent confidence interval, 0.66 to 1.13; P = 0.29). Long-term treatment with trandolapril in patients with reduced left ventricular function soon after myocardial infarction significantly reduced the risk of overall mortality, mortality from cardiovascular causes, sudden death, and the development of severe heart failure. That mortality was reduced in a randomized study enrolling 25 percent of consecutive patients screened should encourage the selective use of ACE inhibition after myocardial infarction.
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            Prior Cytomegalovirus Infection Does Not Predict Clinical Outcome after Percutaneous Transluminal Coronary Angioplasty

            Background: A direct association between human cytomegalovirus (HCMV) infection and the development of restenosis after coronary angioplasty has been suggested. The aim of this prospective study was to evaluate the value of HCMV serology in predicting the clinical outcome after percutaneous transluminal coronary angioplasty (PTCA). Methods and Results: 112 patients undergoing elective PTCA were included in the study. HCMV antibody levels were measured by ELISA. Cardiac events within a follow-up period of 6 months after PTCA were defined as (1) progression or recurrence of anginal complaints and/or a positive exercise test; (2) restenosis that required repeat revascularization. 73% of PTCA patients were seropositive for HCMV. Successful PTCA was achieved in a total of 94 patients, who were followed for 6 months. In 31/94 patients (33%) cardiac events occurred and in 15/94 (16%), this could be related to restenosis. We found no statistically significant difference between seropositive and negative patients with respect to anginal complaints or the need for revascularization. There was no evidence of acute reactivation, since titers of anti-HCMV antibodies did not increase after PTCA. Conclusion: This study shows that the clinical outcome after PTCA is not related to the HCMV serostatus of the patient. Therefore, our data do not support the hypothesis that serological markers of HCMV infection are of clinical importance for the assessment of a patient’s individual risk after PTCA. This does not preclude a role for local reactivation of HCMV at the site of angioplasty.

              Author and article information

              S. Karger AG
              December 2001
              10 December 2001
              : 96
              : 2
              : 65-71
              aDepartment of Medicine B, Rigshospitalet, Copenhagen; bDepartment of Medicine and Cardiology A, Aarhus University Hospital, Aarhus; cDepartment of Medicine Y, Bispebjerg Hospital, Copenhagen; dDepartment of Cardiology, Odense University Hospital, Odense; eDepartment of Medicine E, FrederiksbergHospital, Copenhagen, and fDepartment of Medicine E, Herlev Hospital, Copenhagen, Denmark
              47391 Cardiology 2001;96:65–71
              © 2001 S. Karger AG, Basel

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              Page count
              Figures: 1, Tables: 4, References: 21, Pages: 7
              General Cardiology


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