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

Pierre V. Ennezat, Nicolas Lamblin, Frédéric Mouquet, Olivier Tricot, Philippe Quandalle, Valérie Aumégeat, Octave Equine, Olivier Nugue, Benoit Segrestin, Pascal de Groote, Christophe Bauters
DOI: http://dx.doi.org/10.1093/eurheartj/ehn267 1992-1999 First published online: 20 June 2008

Abstract

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.

Keywords
  • Myocardial infarction
  • Ageing
  • Heart failure
  • Ventricular remodelling

Compared with younger patients, the elderly are more likely to develop cardiovascular diseases and die of cardiovascular causes.1 In addition, ageing is associated with cardiovascular system alterations, including an increase in ventricular and vascular stiffness.2,3 After a myocardial infarction (MI), elderly patients are at an increased risk for adverse events including heart failure and death.4,5

Left ventricular (LV) remodelling, the progressive dilation of the LV following MI,6 is also associated with an increased risk of heart failure and death, and contributes to the progression to heart failure in post-MI patients.7

In the present study, we tested the hypothesis that an increased incidence of heart failure in elderly patients following MI is associated with a greater propensity for LV remodelling.

Methods

Study population

REVE (REmodelage VEntriculaire) is a multicenter prospective study investigating the incidence and determinants of LV remodelling after an inaugural acute anterior Q-wave MI.8,9 We enrolled 266 patients between February 2002 and June 2004. Patients were considered eligible if the infarct zone comprised at least three LV segments that were revealed to be akinetic upon pre-discharge echocardiography. Exclusion criteria were: inadequate echographic image quality, age >85 years, life-limiting non-cardiac disease, significant valvular disease, and prior Q-wave MI. Patients who had scheduled for coronary bypass grafts were also excluded.

Echocardiographic examination

Serial echographic examinations were performed at hospital discharge (Day 5–15), 3 months following MI, and 1 year following MI. Echographic data were obtained by experienced ultrasonographers using commercially available second harmonic imaging systems and were recorded on optical discs. All echocardiograms were analysed at the Lille Core Echo Laboratory. Left ventricular volumes and ejection fractions were calculated using a modified Simpson’s rule. Intra- and inter-observer variabilities in the evaluation of left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) have been reported previously.8 To evaluate regional systolic function, the left ventricle was divided according to a 16-segment model, as recommended by the American Society of Echocardiography,10 and the wall motion score index (WMSI) was derived. We measured the following variables from mitral Doppler tracings with the sample volume at the mitral leaflet tips: peak velocity of early rapid filling wave (E), peak flow velocity at atrial contraction (A), E/A ratio, and deceleration time of early filling. Delayed relaxation was defined as an E/A ratio <1 with a deceleration time >220 ms, and we defined an LV-restrictive pattern as an E/A ratio >2 with a deceleration time <150 ms.11 We diagnosed post-MI mitral regurgitation (MR) based on colour-flow Doppler studies in the parasternal and apical views, and the presence of a structurally normal valve. The severity of MR was assessed semiquantitatively based on MR jet area to left atrial area as described previously.12 We classified MR as absent, mild, and moderate/severe. Left atrial volume was calculated using the ellipsoid model.13

Clinical follow-up

We performed clinical follow-up examinations during outpatient visits or by contacting the general practitioner or cardiologist between February 2005 and June 2007. We collected data on death, hospitalization for heart failure (symptoms of dyspnoea or oedema associated with bilateral rales, elevated venous pressure, interstitial or alveolar oedema observable on chest X-ray, or the addition of intravenous diuretics or inotropic medications), recurrent MI (the occurrence of new pathological Q-waves, or onset of ischaemic symptoms or ischaemic ECG changes with typical rise and fall of biochemical markers of MI), and coronary revascularization. The investigators assessing the clinical endpoints were blinded with regard to age and LV remodelling.

Statistical analysis

Continuous variables were described as the mean ± standard deviation or the median with 25th and 75th percentiles when they did not follow a normal distribution. Discrete variables were presented as percentages. The primary endpoint of the study was LVEDV at the 1 year follow-up examination. For the purposes of presentation, we categorized ages into quartiles: <48 years, 48–57 years, 58–71 years, and >71 years; however, statistical analyses were performed using age as a continuous variable. The relationships between age and discrete variables were assessed using the unpaired Student’s t-test. The relationships between age and continuous variables were assessed by linear regression or Spearman regression analysis when appropriate. To illustrate our findings, LV remodelling was defined as a >20% increase in LVEDV between baseline and 1 year follow-up examination; this definition has been used previously to indicate severe remodelling.8,14 Cox proportional hazards analyses were performed to analyse the relationship between age as a continuous variable and different clinical endpoints at the 3 year follow-up examination. Event-free survival curves for heart failure hospitalization were constructed using the Kaplan–Meier method, and statistical differences between curves were assessed by log-rank test. Two-sided P-values of <0.05 were considered statistically significant. P-values were not adjusted for multiple testing; inflation of the experiment type I error was limited by having a pre-specified hypothesis and focusing on one primary endpoint: LVEDV. Sample size calculations were based on a two-sided alpha error of 0.05 and 80% power. On the basis of previous data from our echocardiographic laboratory, we calculated that 250 patients would provide sufficient power to detect a 10% difference in LVEDV at the 1 year follow-up examination between patients in the highest quartile (>71 years) and younger patients. Analyses were performed with SAS software (release 8.2, SAS Institute, Cary, NC, USA).

Results

The baseline characteristics of the 266 patients who formed the study population are shown in Table 1. Among the older patients, there were slightly more women. The distribution of cardiovascular risk factors differed in association with age, with a higher proportion of hypertension in older patients and a higher proportion of current smokers in younger patients. Diabetes mellitus tended to be more frequent in older patients, while younger patients more often had a familial history of coronary artery disease. Creatinine clearance decreased with advancing age. Overall, acute reperfusion therapy was attempted for 83% of the patients. This proportion did not vary substantially with age, but there was a trend towards lower rates of thrombolysis in older patients. There were significantly more older patients in Killip class ≥2. Peak creatinine kinase levels did not differ significantly among the four age groups. There were similarly high rates of coronary angiography, percutaneous coronary intervention (PCI), and stent implantation procedures during hospitalization within all age quartiles. Multivessel coronary artery disease was more frequent in older patients.

View this table:
Table 1

Baseline characteristics of the study population (n = 266) by age groups

All patients (n = 266)Quartile 1: <48 years (n = 66)Quartile 2: 48–57 years (n = 67)Quartile 3: 58–71 years (n = 67)Quartile 4: >71 years (n = 66)P-value
Age (years)58 ± 1441 ± 552 ± 364 ± 476 ± 3
Women, n (%)67 (25)15 (23)13 (19)16 (24)23 (35)0.03
Body mass index (kg/m2)27.0 ± 4.726.9 ± 5.527.1 ± 5.128.4 ± 4.225.7 ± 3.60.42
Hypercholesterolemia, n (%)123 (46)29 (44)30 (45)38 (57)26 (39)0.66
History of hypertension, n (%)120 (45)10 (15)22 (33)39 (58)49 (74)<0.0001
Current smokers, n (%)122 (46)58 (88)43 (64)15 (22)6 (9)<0.0001
Diabetes mellitus, n (%)60 (23)7 (11)14 (21)25 (37)14 (21)0.04
Familial history of CAD, n (%)64 (24)20 (30)20 (30)15 (22)9 (14)0.003
Creatinine clearance (mL/min)93 ± 35121 ± 32102 ± 2984 ± 2561 ± 19<0.0001
Prior angina pectoris, n (%)30 (11)8 (12)6 (9)10 (15)6 (9)0.70
Prior PCI, n (%)11 (4)2 (3)4 (6)4 (6)1 (2)0.78
Initial reperfusion therapy
 Thrombolysis, n (%)142 (53)42 (64)34 (51)38 (57)28 (42)0.02
 Primary PCI, n (%)78 (29)14 (21)23 (34)19 (28)22 (33)0.33
 No reperfusion therapy, n (%)46 (17%)10 (15%)10 (15%)10 (15%)16 (24%)0.06
Time from symptom onset to reperfusion therapy (h)4.0 [2.0–7.0]3.5 [2.0–7.0]4.0 [2.0–8.0]4.0 [2.0–7.0]4.0 [2.3–7.0]0.61
Killip class ≥2, n (%)71 (27)13 (20)10 (15)23 (34)25 (38)0.002
Peak creatinine-kinase (IU/L)2549 [1234–3984]3003 [1462–4739]2558 [1104–3885]2616 [1515–3945]1831 [978–3571]0.06
Coronary angiography during hospitalization, n (%)263 (99)66 (100)67 (100)66 (99)64 (97)0.11
Multivessel CAD, n (%)101 (38)19 (29)21 (31)27 (41)34 (53)0.001
PCI during hospitalization, n (%)235 (89)59 (89)56 (84)62 (94)58 (91)0.52
Stent implantation, n (%)232 (88)59 (89)55 (82)61 (92)57 (89)0.66
  • Creatinine clearance was calculated from the equation of Cockcroft and Gault.

  • CAD, coronary artery disease; PCI, percutaneous coronary intervention.

The major medications used at the time of hospital discharge and during the follow-up examinations are shown in Table 2. Most patients received at least one antiplatelet drug, a betablocker, an angiotensin-converting enzyme (ACE)-inhibitor or an angiotensin II receptor blocker (ARB), and a statin throughout the 3 year follow-up period. Other than beta blockers, which were less frequently prescribed during follow-up examinations in older patients, and aspirin, which was used less at 3 years, the proportions of patients receiving secondary prevention and antiremodelling medications did not vary with age. However, there was a graded positive association between age and the use of diuretics at discharge and during follow-up examinations.

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Table 2

Major medications at hospital discharge and during follow-up by age groups

Quartile 1: <48 yearsQuartile 2: 48–57 yearsQuartile 3: 58–71 yearsQuartile 4: > 71 yearsP-value
Aspirin, n (%)
 Hospital discharge65 (100)65 (97)65 (97)63 (95)0.19
 3 months62 (98)57 (86)59 (92)57 (92)0.43
 1 year52 (88)51 (77)51 (82)43 (74)0.09
 3 years46 (84)47 (76)35 (63)33 (61)0.003
Clopidogrel, n (%)
 Hospital discharge63 (97)62 (93)62 (93)59 (89)0.08
 3 months48 (76)48 (73)46 (72)41 (66)0.18
 1 year29 (49)38 (58)37 (60)30 (52)0.85
 3 years24 (44)26 (42)29 (52)16 (30)0.24
Beta-blockers, n (%)
 Hospital discharge62 (95)64 (96)61 (91)61 (92)0.23
 3 months61 (97)62 (94)58 (91)52 (84)0.005
 1 year57 (97)61 (92)53 (85)47 (81)0.01
 3 years50 (91)55 (89)47 (84)42 (78)0.09
ACE-inhibitors, n (%)
 Hospital discharge63 (97)67 (100)63 (94)63 (95)0.36
 3 months58 (92)64 (97)55 (86)54 (87)0.06
 1 year50 (85)56 (85)52 (84)44 (76)0.11
 3 years44 (80)51 (82)44 (79)40 (74)0.21
ARB, n (%)
 Hospital discharge1 (2)02 (3)00.80
 3 months4 (6)1 (2)4 (6)2 (3)0.81
 1 year6 (10)7 (11)5 (8)9 (16)0.24
 3 years5 (9)9 (15)6 (11)6 (11)0.79
Spironolactone, n (%)
 Hospital discharge3 (5)8 (12)17 (25)7 (11)0.06
 3 months4 (6)7 (11)18 (28)6 (10)0.15
 1 year3 (5)6 (9)14 (23)4 (7)0.34
 3 years3 (5)6 (10)9 (16)3 (6)0.46
Diuretics, n (%)
 Hospital discharge7 (11)15 (22)25 (37)22 (33)0.0002
 3 months5 (8)11 (17)20 (31)25 (40)<0.0001
 1 year4 (7)11 (17)19 (31)25 (43)<0.0001
 3 years3 (5)9 (15)18 (32)25 (46)<0.0001
Statins, n (%)
 Hospital discharge63 (97)67 (100)65 (97)64 (97)0.65
 3 months57 (90)61 (92)61 (95)57 (92)0.74
 1 year56 (95)61 (92)58 (94)52 (90)0.34
 3 years51 (93)55 (89)47 (84)46 (85)0.16
  • ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker.

  • Data expressed as percentages/265 patients at hospital discharge, 255 patients at 3 months, 245 patients at 1 year, and 227 patients at 3 years.

By 1 year following MI, 18 patients had died; an echocardiographic follow-up examination was performed for 215 of the remaining 248 eligible patients (87%). This rate did not differ with age. The baseline characteristics of the 215 patients who underwent echocardiographic follow-up examinations did not differ from those of the 33 patients who did not undergo echocardiographic follow-up examinations (data not shown). Systolic blood pressure did not differ in accordance with age at baseline, but was significantly higher in older patients at 3 months and at 1 year. Diastolic blood pressure was similar for all three time points. As a result, pulse pressure was significantly higher in older patients at 3 months and at 1 year. Echocardiographic data are summarized in Table 3. Overall, LV remodelling was documented by an increase in LVEDV from 56.4 ± 14.7 mL/m2 at baseline to 62.8 ± 18.7 mL/m2 at 1 year (P < 0.0001) and by an increase in LVESV from 28.7 ± 10.2 mL/m2 at baseline to 31.4 ± 13.7 mL/m2 at 1 year (P = 0.0002). As shown in Table 3, LVEDV and LVESV did not differ with age at any of the three time points. When LV remodelling was defined as a >20% increase in LVEDV from the baseline to 1 year, we observed it in 31, 26, 34, and 34% of patients <48, 48–57, 58–71, and >71 years of age, respectively (P = 0.43) (Figure 1A). In an attempt to avoid potential bias due to the deaths of patients with severe LV remodelling before echocardiographic follow-up examinations could be carried out, we performed a second analysis using death or LV remodelling as the endpoint. As shown in Figure 1B, similar results were observed. The LV ejection fraction was slightly lower in elderly patients at baseline, but did not differ with age at the 3-month or at 1 year follow-up examination. Wall motion score index was similar among the age groups for all three time points. While the frequency of the LV-restrictive filling pattern was similar among the groups for all three time points, a delayed relaxation pattern was more frequently observed in older patients at baseline, 3 months, and 1 year. The prevalence of moderate/severe MR at 1 year was higher in older patients. Left atrial volumes were higher in older patients at discharge and during follow-up examinations.

Figure 1

(A) Left ventricular remodelling (>20% increase in LVEDV between baseline and 1 year) according to age. (B) Death or left ventricular remodelling according to age.

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Table 3

Echocardiographic follow-up at baseline, 3 months, and 1 year by age groups (n = 215 patients with 1 year follow-up)

Quartile 1:<48 yearsQuartile 2:48–57 yearsQuartile 3:58–71 yearsQuartile 4:>71 yearsP-value
Heart rate (b.p.m.)
 Baseline, n = 21466 ± 1067 ± 1269 ± 1168 ± 110.14
 3 months, n = 19563 ± 1165 ± 1166 ± 1263 ± 120.97
 1 year, n = 21565 ± 967 ± 1065 ± 1363 ± 110.13
Systolic BP (mmHg)
 Baseline, n = 214111 ± 19111 ± 15115 ± 16115 ± 140.14
 3 months, n = 182116 ± 14124 ± 16128 ± 17132 ± 22<0.0001
 1 year, n = 207122 ± 16127 ± 17131 ± 18137 ± 26<0.0001
Diastolic BP (mmHg)
 Baseline, n = 21465 ± 1269 ± 1265 ± 1367 ± 100.93
 3 months, n = 18270 ± 1274 ± 1176 ± 1074 ± 120.06
 1 year, n = 20772 ± 1275 ± 1377 ± 1277 ± 150.15
Pulse pressure (mmHg)
 Baseline, n = 21446 ± 1342 ± 950 ± 1747 ± 110.07
 3 months, n = 18246 ± 850 ± 1152 ± 1258 ± 16<0.0001
 1 year, n = 21450 ± 1152 ± 1254 ± 1461 ± 16<0.0001
LVEDV (mL/m2)
 Baseline, n = 21555.4 ± 15.059.0 ± 15.956.3 ± 14.354.5 ± 13.60.42
 3 months, n = 18961.0 ± 15.558.9 ± 15.659.3 ± 15.758.0 ± 16.50.26
 1 year, n = 21561.0 ± 18.263.4 ± 20.065.5 ± 18.761.0 ± 17.80.94
LVESV (mL/m2)
 Baseline, n = 21527.0 ± 8.629.6 ± 11.528.9 ± 9.829.1 ± 10.80.40
 3 months, n = 18929.7 ± 10.728.9 ± 11.329.4 ± 10.829.2 ± 13.20.75
 1 year, n = 21529.8 ± 11.831.2 ± 15.032.9 ± 13.931.5 ± 14.00.39
LVEF (%)
 Baseline, n = 21551.7 ± 7.850.4 ± 10.449.0 ± 8.647.4 ± 10.50.02
 3 months, n = 18952.1 ± 8.151.9 ± 9.050.9 ± 9.350.3 ± 10.40.33
 1 year, n = 21552.0 ± 8.952.4 ± 9.751.1 ± 9.049.9 ± 10.30.15
WMSI
 Baseline, n = 2121.83 ± 0.141.86 ± 0.171.88 ± 0.161.87 ± 0.160.09
 3 months, n = 1891.74 ± 0.201.77 ± 0.171.76 ± 0.201.75 ± 0.190.58
 1 year, n = 2091.66 ± 0.221.70 ± 0.201.72 ± 0.201.74 ± 0.220.06
Delayed relaxation
 Baseline, n = 2110 2 (4%) 5 (9%) 7 (14%)0.002
 3 months, n = 1843 (7%) 4 (8%) 8 (17%)17 (39%)<0.0001
 1 year, n = 2105 (10%)10 (18%)10 (18%)23 (47%)<0.0001
LV restrictive pattern
 Baseline, n = 2135 (10%) 4 (7%) 4 (7%) 2 (4%)0.41
 3 months, n = 1842 (4%) 3 (6%) 1 (2%) 1 (2%)0.17
 1 year, n = 2103 (6%) 1 (2%) 2 (4%) 5 (10%)0.37
Moderate/severe MR
 Baseline, n = 2143 (6%) 6 (11%) 3 (5%) 8 (16%)0.12
 3 months, n = 1894 (8%) 3 (6%) 2 (4%) 6 (13%)0.50
 1 year, n = 2122 (4%) 2 (4%) 4 (7%) 8 (16%)0.005
LA volume (mL/m2)
 Baseline, n = 20923.4 ± 6.025.9 ± 7.626.3 ± 9.727.8 ± 10.30.004
 3 months, n = 18625.8 ± 8.626.8 ± 8.129.3 ± 10.629.7 ± 11.40.03
 1 year, n = 20626.3 ± 8.027.0 ± 8.628.5 ± 11.031.2 ± 11.90.004
  • LVEDV indicates left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; LA, left atrial.

Clinical follow-up data were obtained for 263 patients at a median of 1184 days. Prior to the final follow-up examination, 23 patients were hospitalized for heart failure and 31 patients died. Left ventricular end-diastolic volumes were greater in patients who had been hospitalized for heart failure (baseline, 59.5 ± 14.0 mL/m2; 3 months, 75.0 ± 18 mL/m2; and 1 year, 78.4 ± 20 mL/m2) than in patients who had not been hospitalized for heart failure (baseline, 56.3 ± 15.0 ml/m2; 3 months; 58.5 ± 15.9 mL/m2; and 1 year: 61.7 ± 18.2 ml/m2); P = 0.36, 0.001, and 0.001, for baseline, 3 months, and 1 year, respectively. As shown in Table 4, death and hospitalization for heart failure were more frequent in older patients (P = 0.009 and 0.0002, respectively). Kaplan–Meier curves for hospitalization for heart failure are shown in Figure 2; event-free survival was lower in older patients (P = 0.0002).

Figure 2

Kaplan–Meier survival curves for hospitalization for heart failure according to age.

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Table 4

Actuarial event rates at 3 years by age groups

Quartile 1: <48 years (%)Quartile 2: 48–57 years (%)Quartile 3: 58–71 years (%)Quartile 4: >71 years (%)P-value
Death7.8013.916.90.009
Cardiac death7.806.312.20.17
Hospitalization for HF1.91.511.020.30.0001
Recurrent MI6.86.14.68.10.96
Coronary revascularization21.715.424.222.60.34
  • HF indicates heart failure; MI, myocardial infarction.

Discussion

Our results confirm that age is a major determinant of hospitalization for heart failure after an MI, and extend this finding to elderly patients with no prior history of MI, who underwent acute reperfusion and PCI in most cases and received optimal antiremodelling therapy. Our results also demonstrate that post-MI LV dilation is of the same magnitude in young and old individuals, thereby excluding increased LV remodelling as a causative agent of increased heart failure risk in the elderly. Finally, our results suggest that some of the characteristics of the ageing heart may lead to an altered adaptative response after an MI and, consequently, to an increased risk of heart failure.

The increased risk of heart failure in elderly patients following an acute coronary syndrome is well established,5,1517 and could be explained potentially by several factors: First, elderly patients more often present with a prior history of MI,16,17 which could explain an already depressed LV function at baseline. Secondly, MI size could be greater in elderly patients, due to the fact that they often present with atypical symptoms resulting in longer pre-hospital delays,5,18 or due to underutilization of reperfusion therapy.5,19 Thirdly, elderly patients may be less likely to receive optimal antiremodelling treatments such as ACE inhibitors and beta-blockers after an MI. Fourthly, more severe coronary artery disease in elderly patients may explain more frequent recurrent MI with further decreases in LV function and subsequent heart failure. However, none of these potential explanations account for the marked increase in heart-failure risk that we observed in the present study. Patients with a prior history of MI were not included in our study. The rates of acute reperfusion and PCI during hospitalization were high and similar among the age groups. Infarct size estimated by the peak CK and the WMSI did not differ with age. That beta-blockers are less likely to be prescribed to older patients may have played a role, but it is not likely that this was the sole explanation, since the proportion of elderly patients discharged with ACE inhibitors and beta-blockers was still quite high. Multivessel coronary artery disease was more frequent in older patients, but the rate of recurrent MI was relatively low and similar across age quartiles. Our results therefore suggest that differences in rates of prior events or medical management cannot be the sole explanations for the poorer clinical outcome of elderly patients.

Progressive LV dilation is a strong predictor of heart failure and cardiovascular death after an MI.6,7 Although it was recently shown that LV remodelling can occur in elderly patients despite moderate infarct size and optimized treatment,20 as yet, no study has directly investigated the role of age in post-MI LV remodelling. The strength of our study is that we combined clinical data with quantitative data obtained from systematic follow-up examinations. Left ventricular volumes did not differ with age, and we observed similar rates of LV dilation across all age quartiles. Our results therefore suggest that the association of age with heart failure is not related to increased LV remodelling.

Old age is associated with significant cardiovascular and renal changes2,3,21,22 that might predispose patients to heart failure after an MI. Average systolic blood pressure rises throughout life, whereas diastolic blood pressure tends to level off or decline after 55–60 years of age, resulting in an increase in pulse pressure. Elevated pulse pressure, a marker of vascular stiffening, confers a higher risk of cardiac failure.23 Moreover, normal ageing is associated with alterations in LV diastolic performance,21 which also predispose patients to heart failure. The rise in left atrial volume reflects a preload that is chronically heightened and thereby the severity of diastolic dysfunction. Furthermore, left atrial volume has been shown to be an important predictor of post-MI survival.24 The presence of ischaemic MR, which is correlated with ageing, is likely to worsen left atrial enlargement.25 It has also been reported that after an MI, any renal dysfunction correlates with a poor clinical outcome, including a higher risk of heart failure;26 in addition, renal impairment correlates with increased left atrial volume.27 Vascular stiffening and the higher prevalence observed with old age in our study of impaired LV relaxation, ischaemic MR, higher left atrial volume, and impaired renal function are consistent with the hypothesis that theses changes may limit the adaptation of the ageing heart to acute MI and explain the higher risk of heart failure.

Several limitations need to be addressed: first, this was a retrospective study; however, the echocardiographic follow-up was designed prospectively. Secondly, we cannot exclude the possibility that patients who died prior to the 1 year echocardiographic follow-up examination would have experienced significant LV remodelling. This limitation is inherent in all LV remodelling studies; however, we did not find that age had a substantial effect on the combined endpoint of death or LV remodelling after 1 year. Thirdly, our results were obtained in selected patients with anterior MI and might not apply to all patients after an MI. Fourthly, patients older than 85 years of age were not included in our study; thus, our results may not apply to patients over 85 years of age. Fifthly, when the present study began, B-type natriuretic peptide levels and other non-invasive measures of diastolic function, such as tissue Doppler imaging, were not routinely obtained in the majority of centres, and thus were not available in the entire patient cohort.

In conclusion, in patients with a modern treatment of MI including coronary revascularization, ACE inhibitors, and beta-blockers, we did not find that age had a significant effect on LV remodelling following an MI. Further studies targeting ventricular and vascular stiffening are needed to clarify mechanisms that could explain the more frequent progression to heart failure observed after an MI in elderly patients. Finally, the relationship between poor outcome and ageing indicates that closer attention should be paid to ageing patients after an MI. Thorough clinical follow-up examinations and maximally tolerated doses of medications such as beta-blockers are needed to decrease the rate of heart failure in this high-risk population.

Funding

This study was supported by the Centre Hospitalier Régional et Universitaire de Lille Programme Hospitalier de Recherche Clinique 2001R/1918 and the Fondation de France, Paris.

Acknowledgements

The authors wish to thank Eleni Pelecanos, Michel Deneve, and Stéphane Dequand for study monitoring and for their help in the Lille Core Echo Laboratory.

Conflict of interest: none declared.

References

References

The above article uses a new reference style being piloted by the EHJ that shall soon be used for all articles.

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