The effect of ageing on cardiac remodelling and hospitalization for heart failure after an inaugural anterior myocardial infarction.

AIMS: Following myocardial infarction (MI), both age and left ventricular (LV) remodelling are associated with an increased risk of adverse events. We tested the hypothesis that the increased incidence of heart failure following MI in elderly patients is associated with a greater propensity for LV remodelling. METHODS AND RESULTS: We monitored 266 patients with anterior MI. Echocardiographic studies were performed at hospital discharge, at 3 months, and at 1 year following hospitalization for MI. A clinical follow-up examination was performed after 3 years. Left ventricular remodelling was documented by an increase in LV end-diastolic volume after 1 year. Left ventricular end-diastolic and end-systolic volumes did not differ with age for all time points studied. Left ventricular remodelling was observed in 31, 26, 34, and 34% of patients <48, 48-57, 58-71, and >71 years of age, respectively. The 3 year heart-failure hospitalization rates were 1.9, 1.5, 11.0, and 20.3% for patients <48, 48-57, 58-71, and >71 years of age, respectively. Hospitalization for heart failure was more frequent in older patients. CONCLUSION: We found that age was a major determinant of subsequent re-hospitalization for heart failure. However, we found no significant association between age and the LV remodelling process.

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.

Relation of admission white blood cell count to left ventricular remodeling after anterior wall acute myocardial infarction.

We investigated whether a high white blood cell (WBC) count on admission for acute myocardial infarction (AMI) may be associated with a higher risk of subsequent left ventricular (LV) remodeling. We included 107 patients with anterior AMI. Echocardiographic studies were performed at hospital discharge, at 3 months, and at 1 year after AMI. LV remodeling (>20% increase in end-diastolic volume) was observed in 27% of patients. WBC counts during hospitalization were higher in patients who subsequently underwent LV remodeling (p = 0.003 for WBC count on admission). The increase in end-diastolic volume from baseline to 1 year was greater for patients in the higher tertile of WBC count on admission (p = 0.04). When adjusting for baseline clinical and echocardiographic characteristics by multivariate analysis, WBC count on admission was independently associated with LV remodeling (odds ratio 1.23, 95% confidence interval 1.04 to 1.45, p = 0.018). In conclusion, a high WBC count on admission for AMI is an independent predictor of LV remodeling, even when predischarge echocardiographic variables are taken into account.

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.

Aspirin does not adversely affect survival in patients with stable congestive heart failure treated with Angiotensin-converting enzyme inhibitors.

BACKGROUND: Experimental studies and retrospective analyses of mortality trials with angiotensin-converting enzyme inhibitors (ACE-Is) have suggested that aspirin may reduce the beneficial effect of these drugs. The aim of this study was to assess a possible detrimental effect of aspirin on survival in stable patients with left ventricular systolic dysfunction who had congestive heart failure and had been treated with ACE-Is. METHODS AND RESULTS: We performed a retrospective analysis in 755 consecutive stable patients with left ventricular systolic dysfunction. A Cox regression model was used to select independent predictors of survival and to test for a possible interaction between aspirin and ACE-Is with an adjustment to differences in clinical characteristics in subgroups of patients. Of the 755 patients, 328 (43.4%) had proven ischemic cardiomyopathy, 693 patients (91.8%) were receiving ACE-Is, and 317 patients were receiving aspirin (mean [+/- SD] dose, 183 +/- 65 mg/d; 74% of the patients receiving < or = 200 mg/d). During a median follow-up period of 1,996 days, there were 273 cardiac-related deaths, 14 urgent transplantations, 71 nonurgent transplantations, and 46 noncardiac-related deaths, and 3 patients were lost to follow-up. The cardiovascular mortality rates were 11.5% and 19.0%, respectively, at 1 and 2 years. There were no interactions among aspirin, ACE-Is, and survival in the overall population (p = 0.21), or in subgroups of patients with ischemic cardiomyopathy (p = 0.41) or with nonischemic cardiomyopathy (p = 0.74). CONCLUSIONS: In this population of stable patients with left ventricular systolic dysfunction, our retrospective analysis did not demonstrate any interaction between the use of aspirin and survival in patients receiving ACE-Is.