Secondary medical prevention and clinical outcome in coronary artery disease patients with a history of non-coronary vascular intervention: A report from the CORONOR investigators.

AIM: To assess the level of secondary prevention and the outcome of coronary artery disease (CAD) in patients who have a history of non-coronary vascular intervention. BACKGROUND: Patients with polyvascular disease have been reported to receive less evidence-based medications, with worse risk factor control and to be at higher risk than patients with single-bed disease. It is unknown whether these findings remain valid in the modern era of secondary prevention. METHODS: We included 4184 patients with stable CAD. Two groups were formed according to the absence (n = 3704) or presence (n = 480) of a history of non-coronary vascular intervention. Treatments and risk factor control were recorded at inclusion. Follow-up was performed after 2 years. RESULTS: Antiplatelets, angiotensin system antagonists, beta-blockers and statins were widely prescribed in both groups. The number of antihypertensive drugs was higher in patients with non-coronary vascular intervention. Except for slight increases in the rate of current smokers and in systolic blood pressure, risk factor control was similar between groups. All-cause and cardiovascular mortality rates were higher in patients with non-coronary intervention with adjusted HR of 1.55 (1.13-2.13) (p = 0.007), and 1.98 (1.24-3.15) (p = 0.004), respectively. CONCLUSIONS: In modern practice and real life conditions, the higher risk of CAD patients with a history of non-coronary vascular intervention is taken into account, with more intense secondary prevention and similar risk factor control than patients without such history. In spite of the level of secondary prevention, patients with a history of non-coronary vascular intervention remain at high risk of cardiovascular events. This should be an incentive to discuss more stringent objectives for secondary prevention in patients with polyvascular disease.

Usefulness of serial assessment of B-type natriuretic peptide, troponin I, and C-reactive protein to predict left ventricular remodeling after acute myocardial infarction (from the REVE-2 study).

Left ventricular (LV) remodeling after myocardial infarction (MI) indicates a high risk of heart failure and death. However, LV remodeling is difficult to predict, and limited information is available on the association of cardiac biomarkers with LV remodeling. Our aim was to study the association of B-type natriuretic peptide (BNP), cardiac troponin I (cTnI), and C-reactive protein with LV remodeling after MI. We designed a prospective multicenter study including 246 patients with a first anterior Q-wave MI. Serial echocardiographic studies were performed at hospital discharge and 3 months and 1 year after MI; quantitative analysis was performed at a core echocardiographic laboratory. Blood samples for determination of BNP, cTnI, and C-reactive protein levels were obtained at hospital discharge and the 1-month, 3-month, and 1-year follow up visits. One-year echocardiographic follow-up was obtained in 226 patients. End-diastolic volume increased from 52.3 ± 13.8 ml/m(2) at baseline to 62.3 ± 18.4 ml/m(2) at 1 year (p <0.0001); LV remodeling (>20% increase in end-diastolic volume) was observed in 87 patients (38%). At baseline, we found significant univariate relations between LV remodeling and the 3 biomarkers. During follow-up, high BNP levels and persistently detectable levels of cTnI were associated with LV remodeling. In multivariate analysis, none of the 3 biomarkers at baseline was independently predictive of LV remodeling. In contrast, during follow-up, high BNP and positive cTnI were independently associated with LV remodeling. In conclusion, circulating cardiac biomarkers may reflect pathophysiologic processes implicated in LV remodeling after MI. Determination of BNP and cTnI during follow-up can help refine risk stratification.

Left ventricular remodeling is associated with the severity of mitral regurgitation after inaugural anterior myocardial infarction--optimal timing for echocardiographic imaging.

BACKGROUND: Although mitral regurgitation (MR) has been associated with an increased risk of death and heart failure after myocardial infarction (MI), the relationship between post-MI MR and left ventricular (LV) remodeling has not been entirely clarified. In addition, the optimal timing for assessing MR after MI remains unknown. METHODS: Post-MI MR was assessed by Doppler echocardiography at hospital discharge (baseline) and after 3 months in 261 patients with an inaugural anterior MI. We studied LV remodeling during a 1-year period and clinical follow-up after 3 years, according to MR severity at baseline and at 3 months. RESULTS: Left ventricular remodeling was demonstrated as an increase in LV end-diastolic volume from 56 +/- 15 mL/m(2) at baseline to 63 +/- 19 mL/m(2) at 1 year (P < .0001). MR severity at baseline was not significantly associated with LV remodeling. By contrast, MR severity at 3 months was a strong indicator of LV remodeling. There was a graded increase in the proportion of patients with a >20% increase in LV end-diastolic volume between baseline and 1 year according to MR severity at 3 months (no MR: 21%, mild MR: 32%, moderate/severe MR: 60%) (P = .008). Both MR at baseline and at 3 months were associated with death or rehospitalization for heart failure by univariate analysis (P = .014 and P < .0001, respectively). By multivariable analysis, MR at baseline was not an independent predictor of adverse outcome (P = .66). By contrast, MR at 3 months was independently associated with adverse outcome with a hazard ratio of 2.23 (1.02-4.91 [P = .04]). CONCLUSIONS: After an inaugural anterior MI, MR is associated with LV remodeling and adverse clinical outcome. For prognostic purpose, the optimal timing for assessing MR is the chronic post-MI stage rather than the early post-MI period.

Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group).

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. We enrolled 266 patients with anterior wall Q-wave AMI who had >or=3 segments of the infarct zone that were akinetic on echocardiography before discharge. Echocardiographic follow-up was performed 3 months and 1 year after AMI. LV volumes, ejection fraction, wall motion score index, and mitral flow velocities were determined in a blinded analysis at a core echocardiographic laboratory. Acute reperfusion was attempted in 220 patients (83%; primary angioplasty in 29% and thrombolysis in 54%). During hospitalization, 99% of patients underwent coronary angiography and 87% underwent coronary stenting of the infarct-related lesion. At 1 year, 95% of patients received an antiplatelet agent, 89% a beta blocker, 93% an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, and 93% a statin. Echocardiographic follow-up was obtained in 215 patients. There was recovery in LV systolic function as shown by a decrease in wall motion score index and an increase in ejection fraction. There was a significant increase in end-diastolic volume (EDV; 56.4 +/- 14.7 ml/m2 at baseline, 59.3 +/- 15.7 ml/m2 at 3 months, 62.8 +/- 18.7 ml/m2 at 1 year, p <0.0001). LV remodeling (>20% increase in EDV) was observed in 67 patients (31%). Peak creatine kinase level, systolic blood pressure, and wall motion score index were independently associated with changes in EDV. In conclusion, recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI.