Cardiac remodeling following reperfused acute myocardial infarction is linked to the concomitant evolution of vascular function as assessed by cardiovascular magnetic resonance

Abstract

BackgroundLeft ventricular (LV) remodeling following acute myocardial infarction (MI) is difficult to predict at an individual level although a possible interfering role of vascular function has yet to be considered to date. This study aimed to determine the extent to which this LV remodeling is influenced by the concomitant evolution of vascular function and LV loading conditions, as assessed by phase-contrast Cardiovascular Magnetic Resonance (CMR) of the ascending aorta.MethodsCMR was performed in 121 patients, 2–4 days after reperfusion of a first ST-segment elevation myocardial infarction and 6 months thereafter. LV remodeling was: (i) assessed by the 6-month increase in end-diastolic volume (EDV) and/or ejection fraction (EF) and (ii) correlated with the indexed aortic stroke volume (mL.m−2), determined by a CMR phase-contrast sequence, along with derived functional vascular parameters (total peripheral vascular resistance (TPVR), total arterial compliance index, effective arterial elastance).ResultsAt 6 months, most patients were under angiotensin enzyme converting inhibitors (86%) and beta-blockers (84%) and, on average, all functional vascular parameters were improved whereas blood pressure levels were not. An increase in EDV only (EDV+/EF-) was documented in 17% of patients at 6 months, in EF only (EDV-/EF+) in 31%, in both EDV and EF (EDV+/EF+) in 12% and neither EDV nor EF (EDV-/EF-) in 40%. The increase in EF was mainly and independently linked to a concomitant decline in TPVR (6-month change in mmHg.min.m2.L−1, EDV-/EF-: +1 ± 8, EDV+/EF-: +3 ± 9, EDV-/EF+: -7 ± 6, EDV+/EF+: -15 ± 20, p < 0.001) while the absence of any EF improvement was associated with high persisting rates of abnormally high TPVR at 6 months (EDV-/EF-: 31%, EDV+/EF-: 38%, EDV-/EF+: 5%, EDV+/EF+: 13%, p = 0.007). By contrast, the 6–month increase in EDV was mainly dependent on cardiac as opposed to vascular parameters and particularly on the presence of microvascular obstruction at baseline (EDV-/EF-: 37%, EDV+/EF-: 76%, EDV-/EF+: 38%, EDV+/EF+: 73%, p = 0.003).ConclusionLV remodeling following reperfused MI is strongly influenced by the variable decrease in systemic vascular resistance under standard care vasodilating medication. The CMR monitoring of vascular resistance may help to tailor these medications for improving vascular resistance and consequently, LV ejection fraction.Trial registration NCT01109225 on ClinicalTrials.gov site (April, 2010).

Impact of microvascular obstruction on left ventricular local remodeling after reperfused myocardial infarction

“…Only patients with single‐vessel disease were included. Detailed inclusion/exclusion criteria were presented previously . The study protocol was approved by the local Ethics Committee (CPP agreement #2009‐A00537‐50) and was registered on the http://ClinicalTrials.gov site (NCT01109225).…”

Plasma Galectin-3 predicts deleterious vascular dysfunction affecting post-myocardial infarction patients: An explanatory study

“…As previously described in detail for this "REMI" (relation between aldosterone and cardiac REmodeling after Myocardial Infarction) cohort [1], patients successfully treated by primary percutaneous transluminal coronary angioplasty for a first MI and with an initial occlusion or sub-occlusion of the MI-related coronary artery at angiography, were prospectively included. Main exclusion criteria were: any other significant cardiac disease, any contraindication to MRI, absence of sinus cardiac rhythm, a multivessel disease at coronary angiography, and a >12h delay-time between the onset of chest pain and reperfusion.…”

“…In the previous "REMI" (relation between aldosterone and cardiac REmodeling after Myocardial Infarction) cohort, a lower recovery in cardiac function was documented in patients for whom systemic vascular resistances (SVR) were abnormally high during the post-myocardial infarction (MI) healing period, independently of MI severity and in spite of the commonly prescribed vasodilator regimens (Angiotensin Converting Enzyme Inhibitors (ACEI) or Angiotensin Receptor Blockers (ARBs)) [1]. Such patients with high SVR may be difficult to detect after MI, as well as in the more general setting of heart failure, hypertension being frequently masked by decreases in cardiac contractility and stroke volume [1,2]. In these situations, it is likely that SVR measurements by non-invasive techniques [1][2][3][4] may help in assessing the usefulness of further decreasing SVR by vasodilating treatments.…”

“…Such patients with high SVR may be difficult to detect after MI, as well as in the more general setting of heart failure, hypertension being frequently masked by decreases in cardiac contractility and stroke volume [1,2]. In these situations, it is likely that SVR measurements by non-invasive techniques [1][2][3][4] may help in assessing the usefulness of further decreasing SVR by vasodilating treatments. Such decreases in SVR were indeed previously shown to provide proportional enhancements in cardiac output after MI [5].…”

“…In light of the above, this ancillary and exploratory analysis of the "REMI" post-MI cohort [1] was aimed at characterizing those patients suffering from high SVR remotely from MI with a large a panel of cardiovascular MRI parameters and blood biomarkers.…”