Changes of matrix metalloproteinase-9 level is associated with left ventricular remodeling following acute myocardial infarction among patients treated with trandolapril, valsartan or both.

BACKGROUND: Inhibition of the renin-angiotensin system (RAS) with angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) can suppress left ventricular (LV) remodeling after acute myocardial infarction (AMI), possibly through the modifications of matrix metalloproteinase (MMP)-9. Whether LV remodeling is suppressed in association with MMP-9 suppression in post-AMI/-percutaneous coronary intervention (PCI) patients treated with ACE inhibitor and/or ARB was examined. The presence of any differences in LV remodeling and MMP-9 levels across the groups was also investigated. METHODS AND RESULTS: Sixty-five patients were initiated into each of 3 treatments; trandolapril, valsartan or a combination of both (half-dose-trandolapril plus half-dose-valsartan). Changes in MMP-9, LV end-diastolic and end-systolic volume index (LVEDVI and LVESVI) after 12 months were assessed. Overall, MMP-9 significantly decreased, although neither LVEDVI nor LVESVI increased significantly. DeltaMMP-9 was significantly correlated with DeltaLVEDVI (r=0.36) or DeltaLVESVI (r=0.39). In comparison, across groups, it was found that MMP-9, LVEDVI and LVESVI at 12 months were significantly lower in the combination therapy group than in the trandolapril group. There were no significant differences between the valsartan group and combination therapy group, or between the valsartan group and the trandolapril group. CONCLUSIONS: LV remodeling might be suppressed in association with MMP-9 suppression in AMI patients treated with PCI and regular dose or half-dose-combination of RAS inhibitors. Furthermore, a half-dose-combination might suppress LV remodeling more effectively than trandolapril alone.

Relationship between coronary artery wall thickness measured by 64-slice multidetector computed tomography and cardiovascular risk factors.

BACKGROUND: Recent studies have demonstrated the quantitative ability of contrast-enhanced multidetector computed tomography (MDCT) to evaluate not only the vessel lumen but also coronary plaque. The aim of this study was to assess the association between coronary wall thickness quantified by 64-slice MDCT and cardiovascular risk factors. METHODS AND RESULTS: A total of 149 subjects with suspected coronary artery disease were scanned by contrast-enhanced 64-slice MDCT. The maximum coronary wall thickness of each proximal segment was measured and associations with baseline coronary risk factors were analyzed. The mean maximum wall thickness of all 149 patients was 0.7+/-0.3 mm and there was a significant positive correlation with age (P<0.001) and hemoglobin (Hb) A1c (P=0.001). Patients with hypertension (0.8+/-0.3 vs 0.7+/-0.3 mm, P=0.024) and diabetes (0.9+/-0.4 vs 0.7+/-0.3 mm, P=0.002) had thicker walls than those without. Multivariate linear regression analysis demonstrated that both risk factors were independently correlated with mean maximum wall thickness. CONCLUSIONS: Coronary wall thickness measured by 64-slice MDCT is associated with age and HbA1c, so may add useful information to cardiovascular risk stratification.

Therapy with statins and aspirin enhances long-term outcome of percutaneous coronary intervention.

Aspirin is the standard therapy applied after coronary intervention, and statins are also prescribed to prevent secondary coronary heart disease. We assessed the ability of a combination of statins and aspirin to improve the longterm prognosis of patients after percutaneous coronary intervention (PCI). We collected data from 575 consecutive patients who underwent PCI. The patients were divided into groups depending on the presence or absence of statin or aspirin therapy as follows: both statin and aspirin (Group B: n = 190; 33%); aspirin only (Group A: n = 236; 41.1%); statin only (Group S: n = 53; 9.2%S); neither drug (Group N: n = 96; 16.7%). Data were statistically assessed using the Cox proportional hazard model for multivariate analysis with adjustment of baseline convariates. Sixty-eight patients died during follow-up (11 +/- 3 years). Multivariate analysis showed that compared with group N, both groups S and A were independent predictors for survival from all causes [group S: hazards ratio (HR) 0.29, 95% confidence interval (CI) 0.10-0.81, P = 0.019; group A: HR 0.31, 95% CI 0.17-0.56, P < 0.0001] and cardiovascular (CV) death (group S: HR 0.16, 95% CI 0.04-0.73, P = 0.018; group A: HR 0.12, 95% CI 0.05-0.30, P < 0.001). risk for all causes and CV death was significantly lower in Group B (HR 0.25, 95% CI 0.12-0.53, P < 0.0001 and HR 0.10, 95% CI 0.03-0.31, P < 0.0001, respectively). Therapy with statins plus aspirin improves long-term clinical outcome in patients after PCI.

Clinical efficacy of benidipine for vasospastic angina pectoris.

BACKGROUND: Most patients with vasospastic angina who have no significant organic coronary arterial stenosis are well controlled by medical therapy and the prognosis is almost satisfactory. Calcium channel (Ca) blockers are used as the first choice and effective agents for vasospastic angina pectoris. However, they do not always work well. Some uncontrolled coronary vasospasms would happen to cause prolonged occlusion of coronary artery resulting in myocardial infarction, life-threatening arrhythmias and sudden death. Therefore, it is very important to pay attention to such a refractory coronary spasm and choose the most effective agent out of Ca blockers for the treatment of each patient with vasospastic angina attacks. This study was designed to evaluate the anti-vasospastic efficacy of benidipine, a long acting dihydropyridine (DHP) Ca blocker, in patients with other Ca blockers-resistant angina. METHODS: Patients treated with diltiazem but not enough to control angina attacks were enrolled in the present study. Treatment with diltiazem (CAS 33286-22-5, 42399-41-7) was changed to treatment with benidipine (CAS 91599-74-5) and the parameters such as angina frequency, duration, blood pressure, heart rate, electrocardiogram and hematological parameters (serum NO(x), plasma cGMP) were measured and compared. RESULTS: Fifteen patients with vasospastic angina were enrolled. After switching from diltiazem to benidipine, angina attacks were completely disappeared in six patients. Although the frequency was not decreased, the average duration of attacks was shorter than before in three patients. Four patients did not improve and two patients obviously worsened. In the improved nine patients, serum nitrite/nitrate (NO(x)) levels showed a significant increase from 37.6 +/- 15.3 to 54.5 +/- 26.7 pmol/L (p < 0.05) and cGMP levels subsequently elevated from 2.2 +/- 0.8 to 2.5 +/- 0.6 micromol/L (p = 0.05) after benidipine therapy started. Adverse effects such as hypotension and bradycardia were not observed. CONCLUSION: This study suggests that benidipine may be helpful in Japanese patients with vasospastic or variant angina pectoris, if diltiazem was not successful.

Long-term (11-year) statin therapy following percutaneous coronary intervention improves clinical outcome and is not associated with increased malignancy.

BACKGROUND: Statins have been proven to reduce cardiac events and mortality. However, there are few studies dealing with the long-term efficacy of statin therapy following percutaneous coronary intervention (PCI). METHODS: We collected data from 575 consecutive patients who underwent PCI between 1987 and 1992. The baseline data, mortality and incidence of cardiovascular events of patients given statins and those not given statins at the time of PCI were compared. RESULTS: There were 243 patients in the statin group and 332 patients in the non-statin group. During follow-up (11.0+/-3.0 years), 68 patients died. At about 10 years, statin use was significantly associated with lower all-cause mortality (8.2% versus 14.5%, P=0.023) and cardiac death (2.5% versus 6.9%, P=0.017). After adjusting for variables, statin use was found to be an independent predictor of death from all causes (hazard ratio [HR] 0.54, 95% confidence interval [CI] 0.29-0.99, P=0.048) and cardiac death (HR 0.24, 95% CI 0.07-0.80, P=0.02). CONCLUSION: Statin use at the time of PCI was associated with a significantly reduced risk of death from all causes and cardiac death. Furthermore, this study provides evidence of a clinical benefit at about 10 years of statin use in patients who underwent PCI.

Impact of aspirin treatment on long-term outcome (over 10 years) after percutaneous coronary intervention.

Aspirin has been shown to reduce cardiovascular morbidity and mortality following percutaneous coronary intervention (PCI). However, its effects on long-term (over 10 years) mortality have not been fully elucidated. This retrospective study recorded the patient characteristics and admission medication for all patients undergoing PCI over an 8-year period from 1984 to 1992. Follow-up information was available for 748 patients (100%) for a mean of 143.6 +/- 43.4 months. A propensity analysis was performed to adjust for presumed selection biases in the administration of aspirin. The baseline clinical characteristics were similar between the group that received aspirin and the group that did not, except for the administration of statins and PCI procedural success rate. Of the 748 patients, 535 (71.5%) received aspirin treatment at the time of PCI. During the 12-year follow-up, 54 patients died from any cause and 20 patients from cardiac death. Kaplan-Meier analysis showed that aspirin treatment led to a significant reduction in all cause mortality (10% versus 16.4%; P = 0.01) and cardiac death (3.7% versus 8.0%; P = 0.02) compared to other antiplatelet drugs. The hazard ratio (HR) for the total mortality and cardiac mortality rates was adjusted using the Cox-proportional hazard model for confounding variables and propensity score. The all cause (HR, 0.49; 95%CI [0.29-0.80], P = 0.005) and cardiac mortality rates (HR, 0.32; 95%CI [0.14-0.72], P = 0.006) for patients receiving aspirin remained lower than for those not receiving aspirin. Aspirin treatment at the time of PCI significantly reduced the risk of death from any cause and cardiac death. The administration of aspirin had a positive impact on the over 10-year long-term outcomes of patients who underwent PCI.