Familial hypercholesterolemia (FH) is relatively prevalent in myocardial infarction (MI) sufferers, and its diagnosis could improve preventive treatment in family members. We aim to analyze the diagnosis of FH and the rate of genetic testing in a prospective cohort of 245 patients submitted to our Cardiac Rehabilitation Program (CRP) after MI. Baseline characteristics were registered, and basal low-density lipoprotein cholesterol (LDL-C) was calculated after correction for lipid-lowering therapies (LLT) before or during admission. Simplified Dutch Lipid Clinic Network Scores (sDLCNS) were retrospectively calculated based on personal and familial history of premature cardiovascular disease and basal LDL-C levels. Mean age was 62.19 ± 13.93 years, and most patients were male (81.6%). Mean LDL-C before admission and basal LDL-C corrected for LLT were 131.79 ± 45.34 mg/dL and 162.87 ± 44.17 mg/dL, respectively. Patients in the cohort were retrospectively categorized in the “unlikely” (<3 points; n = 162, 66.1%), “possible” (3–5 points; n = 72, 29.4%) and “probable” (6–8 points; n = 11, 4.5%) sDLCNS categories. Genetic testing for FH was requested in four (1.6%) patients, and no clinically significant genetic variants were detected. Patients who underwent genetic testing depicted significantly higher basal LDL-C (233 ± 49.09 vs. 161.71 ± 43.25 mg/dL, p = 0.001). However, the rate of individuals undergoing genetic testing was negligible even in the “possible” (n = 2, 2.8%) and “probable” (n = 1, 9.1%) sDLCNS categories. In conclusion, genetic testing for FH in our CRP after MI is largely underutilized, even in patients with a “possible” or “probable” diagnosis based on sDLCNS criteria, which represent about a third of the cohort. Strategies to improve screening for FH should be prospectively implemented.
Background: Exercise-based cardiac rehabilitation programs (CRP) are recommended for patients following acute coronary syndrome to potentially improve high-density lipoprotein cholesterol (HDL-C) levels and prognosis. However, not all patients reach target HDL-C levels. Here we analyze the dynamics and predictors of HDL-C increase during CRP in patients following ST-segment elevation myocardial infarction or occlusion myocardial infarction. Methods: We conducted a prospective study of myocardial infarction patients who completed exercise-based Phase 2 CRP. Data was collected on clinical variables, cardiovascular risk factors, treatment goals, pharmacological therapy, and health outcomes through questionnaires at the beginning and at the end of Phase 2 CRP. Lipid profile analysis was performed before discharge, 4 to 6 weeks after discharge, and at the end of Phase 2 CRP. Changes in lipid profiles were evaluated, and predictors of failure to increase HDL-C levels were identified by binary logistic regression analysis. Results: Our cohort comprised 121 patients (mean age 61.67 ± 10.97 years, 86.8% male, and 47.9% smokers before admission). A significant decrease in total cholesterol, triglycerides, and low-density lipoprotein cholesterol (LDL-C) were noted, along with an increase in HDL-C (43.87 ± 9.18 vs. 39.8 ± 10.03 mg/dL, p < 0.001). Patients achieving normal HDL-C levels (>40 mg/dL in men and >50 mg/dL in women) significantly increased from 34.7% at admission to 52.9% the end of Phase 2. Multivariable analysis revealed smoking history (hazard ratio [HR] = 0.35, 95% confidence interval [CI], 0.11–0.96, p = 0.04), increased reduction in total cholesterol (HR = 0.94, 95% CI, 0.89–0.98, p = 0.004), and increased reduction in LDL-C (HR = 0.94, 95% CI, 0.89–0.99, p = 0.01) were inversely associated with failure to increase HDL-C levels. Conversely, higher HDL-C before CRP (HR = 1.15, 95% CI, 1.07–1.23, p < 0.001) and increased lipoprotein (a) (HR = 1.01, 95% CI, 1–1.02, p = 0.04) predicted failure to increase HDL-C levels. No significant correlations were found with Mediterranean diet adherence, weekly physical activity, training modalities, or physical fitness parameters. Conclusions: Participation in an exercise-based Phase 2 CRP led to mild but significant increases in HDL-C. Smoking history and patients experiencing substantial reductions in total cholesterol and LDL-C were more likely to experience HDL-C increases, unlike those with higher HDL-C and lipoprotein (a) levels before CRP.
BACKGROUND:Left ventricular thrombus (LVTh) is a severe complication after ST-segment elevation myocardial infarction (STEMI). OBJECTIVES:We aim to predict LVTh occurrence by cardiac magnetic resonance (CMR) using clinical, echocardiographic, and electrocardiographic (ECG) variables readily available at admission. METHODS:We included 590 reperfused STEMI patients who underwent early (1-week) and/or late (6-month) CMR in our institution. Baseline clinical, echocardiographic (left ventricular ejection fraction -LVEF-) and ECG data (summatory of ST-segment elevation -sum-STE- and Q-wave and residual ST-elevation >1 mm -Q-STE-) during admission were registered. Multivariate binary logistic regression models and receiver operating characteristic curves were computed for LVTh prediction. RESULTS:LVTh was detected by CMR in 43 (7.3 %) patients and was predicted by previous chronic coronary syndrome (CCS, HR 4.74 [1.82-12.35], p = 0.001), anterior STEMI (HR 10.93 [2.47-48.31], p = 0.002), LVEF (HR 0.96 [0.93-0.99] per %, p = 0.008), maximum sum-STE (HR 1.04 [1.01-1.07] per mm, p = 0.04), and Q-STE (HR 1.31 [1.08-1.6] per lead, p = 0.008). High-risk patients with both major (anterior STEMI and Q-STE in ≥1 leads) and 1-3 minor (CCS, maximum sum-STE >10 mm, LVEF <50%) factors showed the highest LVTh risk (19.6 % within 6 months). The model showed excellent discrimination ability (area under the curve=0.85 [0.81-0.9], p < 0.001). Simplified 4-variable (excluding sum-STE) and 3-variable (also excluding CCS) risk scores showed similar discrimination ability and were externally validated. CONCLUSIONS:LVTh within 6 months post-STEMI can be predicted using pre-discharge clinical (anterior infarction and CCS), echocardiographic (LVEF), and ECG (sum-STE and Q-STE) data. Our results can help select patients who should undergo CMR after STEMI for LVTh detection.
We hypothesized that a short-course high-intensity statin treatment during admission for myocardial infarction (MI) could rapidly reduce LDL-C and thus impact the choice of lipid-lowering therapy (LLT) at discharge. Our cohort comprised 133 MI patients (62.71 ± 11.3 years, 82% male) treated with atorvastatin 80 mg o.d. during admission. Basal LDL-C levels before admission were analyzed. We compared lipid profile variables before and during admission, and LLT at discharge was registered. Achieved theoretical LDL-C levels were estimated using LDL-C during admission and basal LDL-C as references and compared to LDL-C on first blood sample 4–6 weeks after discharge. A significant reduction in cholesterol from basal levels was noted during admission, including total cholesterol, triglycerides, HDL-C, non-HDL-C, and LDL-C (−39.23 ± 34.89 mg/dL, p < 0.001). LDL-C levels were reduced by 30% in days 1–2 and 40–45% in subsequent days (R2 0.766, p < 0.001). Using LDL-C during admission as a reference, most patients (88.7%) would theoretically achieve an LDL-C < 55 mg/dL with discharge LLT. However, if basal LDL-C levels were considered as a reference, only a small proportion of patients (30.1%) would achieve this lipid target, aligned with the proportion of patients with LDL-C < 55 mg/dL 4–6 weeks after discharge (36.8%). We conclude that statin treatment during admission for MI can induce a significant reduction in LDL-C and LLT at discharge is usually prescribed using LDL-C during admission as the reference, which leads to insufficient LDL-C reduction after discharge. Basal LDL-C before admission should be considered as the reference value for tailored LLT prescription.
BackgroundImplantable cardioverter defibrillators (ICD) are effective as a primary prevention measure of ventricular tachyarrhythmias in patients with ST-segment elevation myocardial infarction (STEMI) and depressed left ventricular ejection fraction (LVEF). The implications of using cardiac magnetic resonance (CMR) instead of echocardiography (Echo) to assess LVEF prior to the indication of ICD in this setting are unknown.Materials and methodsWe evaluated 52 STEMI patients (56.6 ± 11 years, 88.5% male) treated with ICD in primary prevention who underwent echocardiography and CMR prior to ICD implantation. ICD implantation was indicated based on the presence of heart failure and depressed LVEF (≤ 35%) by echocardiography, CMR, or both. Prediction of ICD therapies (ICD-T) during follow-up by echocardiography and CMR before ICD implantation was assessed.ResultsCompared to echocardiography, LVEF was lower by cardiac CMR (30.2 ± 9% vs. 37.4 ± 7.6%, p < 0.001). LVEF ≤ 35% was detected in 24 patients (46.2%) by Echo and in 42 (80.7%) by CMR. During a mean follow-up of 6.1 ± 4.2 years, 10 patients received appropriate ICD-T (3.16 ICD-T per 100 person-years): 5 direct shocks to treat very fast ventricular tachycardia or ventricular fibrillation, 3 effective antitachycardia pacing (ATP) for treatment of ventricular tachycardia, and 2 ineffective ATP followed by shock to treat ventricular tachycardia. Echo-LVEF ≤ 35% correctly predicted ICD-T in 4/10 (40%) patients and CMR-LVEF ≤ 35% in 10/10 (100%) patients. CMR-LVEF improved on Echo-LVEF for predicting ICD-T (area under the curve: 0.76 vs. 0.48, p = 0.04).ConclusionIn STEMI patients treated with ICD, assessment of LVEF by CMR outperforms Echo-LVEF to predict the subsequent use of appropriate ICD therapies.
In the setting of acute myocardial infarction (MI), magnetic resonance imaging (MRI) is considered the reference for the quantification of left ventricular ejection fraction (LVEF), infarct size (using late gadolinium enhancement [LGE] extent), and microvascular obstruction (MVO). If MRI can be useful for the diagnostic of MI especially in case of MI with nonobstructive coronary arteries or when there is a doubt about the occurrence of an MI, MRI findings have also a strong prognostic value in patients with recent acute MI. Among MRI parameters, LVEF is recognized as an independent predictor of major adverse cardiovascular events (MACE), while MVO and infarct size were not independents in a large systematic review, but could be combined to further improve MACE prediction. Many other MRI parameters have been proposed: myocardial salvage index, myocardial hemorrhage (using T2 weighted or T2* imaging), native T1 mapping values in the remote myocardium, and oedema extent. A recent expert panel has stratified those MRI findings in the setting of recent MI (5 + 2 days) to highlight those which can be considered as endpoints for experimental studies and clinical trials: LGE extent, MVO, and LVEF are the items to be considered first because they have the most evidence. Despite providing a strong prognostic prediction and eventually other valuable information, MRI is not recommended systematically after an acute MI. According to current guidelines, every patient should have an LVEF assessment by echocardiography, although previous papers have shown the incremental value of LVEF in MRI over echocardiography, MRI cannot be routinely performed due to cost and availability constraints. Thus, additional data are needed to understand for which patients the addition of MRI would be most useful. Even with the dramatic improvement in the treatment of acute treatment of ST-segment elevation myocardial infarction (STEMI), long term incidence of heart failure (HF) is still a major concern. A recent work on 700 patients found a 13.3% incidence rate at 3 years, which triplicate the rate of death, occurring more frequently in older age, diabetes and when echo LVEF <50% at hospital discharge. In the paper published is this issue of JMRI, the authors evaluated the prognostic information of MRI, especially LVEF to predict readmission for HF after a STEMI. Theirs results are based on a registry of 759 patients (among them, 23% were considered elderly, defined by an age >70 years). All patients underwent an MRI at 7 2 days after MI, and 579 also had a follow-up MRI at 3 month. Overall, a reduced LVEF (<40%) was a predictor of acute HF in the whole population whereas a slightly reduced LVEF (41%–49%) was a predictor of acute HF only in the elderly group. In agreement with the literature, MRI LVEF performed better than echo LVEF, MVO, and infarct size after adjustment. LVEF reflects a global decrease in myocardial function and might include previous myocardial damage, this could explain its superiority to predict HF compared with MVO or even infarct size which are only related with MI and do not consider patient past medical history. In addition, elderly patients were at higher risk to transit to lower LVEF state, than non-elderly. To transpose this results in clinical practice, they suggest that a mild reduced LVEF in older patient would require a closer follow-up to detect an impairment in LV systolic function and a higher risk of acute HF. However, the retrospective nature of this fine work limits the authors’ conclusions because they did not assess the impact of MRI on patient management and the
AbstractAimsTraditional adverse events in chronic coronary syndrome (CCS) include atherothrombotic events but usually exclude heart failure (HF). Data are scarce about how new‐onset HF modifies mortality risk. We aimed to determine the incidence of HF and compare its long‐term mortality risk with myocardial infarction (MI) and stroke in patients with known or suspected CCS.MethodsWe prospectively evaluated 5811 consecutive HF‐free patients submitted to vasodilator stress cardiac magnetic resonance (CMR) for known or suspected CCS. Ischaemic burden and left ventricular ejection fraction were assessed by CMR. HF included outpatient diagnosis or acute HF hospitalization. The mortality risk for the incident events and their cross‐comparisons were evaluated using a Markov illness–death model with transition‐specific survival models.ResultsThe mean age was 55 ± 11 years, and 38.9% were female. At a median follow‐up of 5.44 (IQR = 2.53–8.55) years, 591 deaths were registered (1.79 per 100 P‐Y). The rates of new‐onset HF were higher compared with MI and stroke [1.02, 0.62, and 0.51, respectively (P < 0.05)]. The adjusted association between new‐onset HF, MI, and stroke, and subsequent mortality was time dependent. The risk increased almost linearly for HF and became significant by the third year. By Year 10, the mortality risk attributable to new‐onset HF was more than 2.5‐fold (HR: 2.68, 95% CI = 1.74–4.12). For MI, there was a significant increase in mortality risk up to the second year, followed by a monotonic decrease. For stroke, the mortality risk increased for the entire follow‐up but became significant by the third year. A cross‐comparison among incident endpoints HF outnumbers risk for those with MI by the sixth year (HRyear6.3: 1.88, 95% CI = 1.03–3.43). There was no difference in mortality risk between incident HF and stroke.ConclusionsIn patients with CCS, long‐term rates of incident HF were higher than MI and stroke. Patients with new‐onset HF showed a higher risk of long‐term mortality.
Background: Cardiac magnetic resonance (CMR) performed early after ST-segment elevation myocardial infarction (STEMI) can improve major adverse cardiac event (MACE) risk prediction. We aimed to create a simple clinical-CMR risk score for early MACE risk stratification in STEMI patients. Methods: We performed a multicenter prospective registry of reperfused STEMI patients (n = 1118) in whom early (1-week) CMR-derived left ventricular ejection fraction (LVEF), infarct size and microvascular obstruction (MVO) were quantified. MACE was defined as a combined clinical endpoint of cardiovascular (CV) death, nonfatal myocardial infarction (NF-MI) or re-admission for acute decompensated heart failure (HF). Results: During a median follow-up of 5.52 [2.63-7.44] years, 216 first MACE (58 CV deaths, 71 NF-MI and 87 HF) were registered. Mean age was 59.3 +/- 12.3 years and most patients (82.8%) were male. Based on the four variables independently associated with MACE, we computed an 8-point risk score: time to reperfusion >4.15 h (1 point), GRACE risk score > 155 (3 points), CMR-LVEF <40% (3 points), and MVO >1.5 segments (1 point). This score permitted MACE risk stratification: MACE per 100 person-years was 1.96 in the low-risk category (0-2 points), 5.44 in the intermediate-risk category (3-5 points), and 19.7 in the high-risk category (6-8 points): p < 0.001 in multivariable Cox survival analysis. Conclusions: A novel risk score including clinical (time to reperfusion >4.15 h and GRACE risk score > 155) and CMR (LVEF <40% and MVO >1.5 segments) variables allows for simple and straightforward MACE risk stratification early after STEMI. External validation should confirm the applicability of the risk score.
BackgroundMagnetic resonance imaging (MRI) is the most accurate imaging technique for left ventricular ejection fraction (LVEF) quantification, but as yet the prognostic value of LVEF assessment at any time after ST‐segment elevation myocardial infarction (STEMI) for subsequent major adverse cardiac event (MACE) prediction is uncertain.PurposeTo explore the prognostic impact of MRI‐derived LVEF at any time post‐STEMI to predict subsequent MACE (cardiovascular death or re‐admission for acute heart failure).Study TypeProspective.PopulationOne thousand thirteen STEMI patients were included in a multicenter registry.Field Strength/Sequence1.5‐T. Balanced steady‐state free precession (cine imaging) and segmented inversion recovery steady‐state free precession (late gadolinium enhancement) sequences.AssessmentPost‐infarction MRI‐derived LVEF (reduced [r]: <40%; mid‐range [mr]: 40%–49%; preserved [p]: ≥50%) was sequentially quantified at 1 week and after >3 months of follow‐up.Statistical TestsMulti‐state Markov model to determine the prognostic value of each LVEF state (r‐, mr‐ or p‐) at any time point assessed to predict subsequent MACE. A P‐value <0.05 was considered to be statistically significant.ResultsDuring a 6.2‐year median follow‐up, 105 MACE (10%) were registered. Transitions toward improved LVEF predominated and only r‐LVEF (at any time assessed) was significantly related to a higher incidence of subsequent MACE. The observed transitions from r‐LVEF, mr‐LVEF, and p‐LVEF states to MACE were: 15.3%, 6%, and 6.7%, respectively. Regarding the adjusted transition intensity ratios, patients in r‐LVEF state were 4.52‐fold more likely than those in mr‐LVEF state and 5.01‐fold more likely than those in p‐LVEF state to move to MACE state. Nevertheless, no significant differences were found in transitions from mr‐LVEF and p‐LVEF states to MACE state (P‐value = 0.6).Data ConclusionLVEF is an important MRI index for simple and dynamic post‐STEMI risk stratification. Detection of r‐LVEF by MRI at any time during follow‐up identifies a subset of patients at high risk of subsequent events.Level of Evidence2Technical Efficacy Stage2
Residual ST-segment elevation after ST-segment elevation myocardial infarction (STEMI) has traditionally been considered a predictor of left ventricular (LV) dysfunction and ventricular aneurism. However, the implications in terms of long-term prognosis and cardiac magnetic resonance (CMR)-derived structural consequences are unclear. A total of 488 reperfused STEMI patients were prospectively included. The number of Q wave leads with residual ST-segment elevation > 1 mm (Q-STE) at pre-discharge ECG was assessed. LV ejection fraction (LVEF, %) and infarct size (IS, % of LV mass) were quantified in 319 patients at 6-month CMR. Major adverse cardiac events (MACE) were defined as all-cause death and/or re-admission for acute heart failure (HF), whichever occurred first. During a mean follow-up of 6.1 years, 92 MACE (18.9%), 39 deaths and 53 HF were recorded. After adjustment for baseline characteristics, Q-STE (per lead with > 1 mm) was independently associated with a higher risk of long-term MACE (HR 1.24 [1.07–1.44] per lead, p = 0.004), reduced (< 40%) LVEF (HR 1.36 [1.02–1.82] per lead, p = 0.04) and large (> 30% of LV mass) IS (HR 1.43 [1.11–1.85] per lead, p = 0.006) at 6-month CMR. Patients with Q-STE ≥ 2 leads (n = 172, 35.2%) displayed lower MACE-free survival, more depressed LVEF, and larger IS at 6-month CMR ( p < 0.001 for all comparisons). Residual ST-segment elevation after STEMI represents a universally available tool that predicts worse long-term clinical and CMR-derived structural outcomes.
Purpose: Vasodilator stress cardiac magnetic resonance (VS-CMR) has become crucial in the workup of patients with known or suspected chronic coronary syndrome (CCS). Whether traditional exercise ECG testing (ExECG) contributes prognostic information beyond VS-CMR is unclear. Methods: We retrospectively included 288 patients with known or suspected CCS who had undergone ExECG and subsequent VS-CMR in our institution. Clinical, ExECG, and VS-CMR variables were recorded. We defined the serious adverse events (SAE) as a combined endpoint of acute coronary syndrome, admission for heart failure, or all-cause death. Results: During a mean follow-up of 4.2 ± 2.15 yr, we registered 27 SAE (15 admissions for acute coronary syndrome, eight admissions for heart failure, and four all-cause deaths). Once adjusted for clinical, ExECG, and VS-CMR parameters associated with SAE, the only independent predictors were HRmax in ExECG (HR = 0.98: 95% CI, 0.96-0.99; P = .01) and more extensive stress-induced perfusion defects (PDs, number of segments) in VS-CMR (HR = 1.19: 95% CI, 1.07-1.34; P < .01). Adding HRmax significantly improved the predictive power of the multivariable model for SAE, including PDs (continuous reclassification improvement index: 0.47: 95% CI, 0.10-0.81; P < .05). The annualized SAE rate was 1% (if PD < 2 segments and HRmax > 130 bpm), 2% (if PD < 2 segments and HRmax ≤ 130 bpm), 3.2% (if PD ≥ 2 segments and HRmax > 130 bpm), and 6.3% (if PD ≥ 2 segments and HRmax ≤ 130 bpm), P < .01, for the trend. In patients on β-blocker therapy, however, only PDs in VS-CMR, but not HRmax, predicted SAE. Conclusions: We conclude that ExECG contributes significantly to prognostic information beyond VS-CMR in patients with known or suspected CCS.
Objective We assessed the influence of the ischaemic burden (IB) as derived from vasodilator stress cardiovascular magnetic resonance (CMR) on the risk of death and the effect of revascularisation across sex. Methods We evaluated 6237 consecutive patients with known or suspected chronic coronary syndrome (CCS). Extensive ischaemia was defined as >5 segments with perfusion deficit. Multivariate Cox proportional hazard regression models were used. Results A total of 2371 (38.0%) patients were women and 583 (9.3%) underwent CMR-related revascularisation. During a median follow-up of 5.13 years, 687 (11.0%) deaths were reported. We found an adjusted differential effect of CMR-derived IB across sex (p value for interaction=0.039). Women exhibited an adjusted lower risk of death and only equaled men’s risk when extensive ischaemia was present. Likewise, CMR-related revascularisation was shown to be differentially associated with the risk of mortality across sex (p value for interaction=0.025). In patients with non-extensive ischaemia, revascularisation was associated with a higher risk of death, with a greater extent in women. At higher IB, revascularisation was associated with a lower risk in men, with more uncertain results in women. Conclusions CMR-derived IB allows predicting the risk of death and gives insight into the potential effect of revascularisation in men and women with CCS. Compared with men, women with non-extensive ischaemia displayed a lower risk and a similar risk with a higher IB. The impact of CMR-related revascularisation on mortality risk was also significantly different according to IB and sex. Further research will be needed to confirm these hypothesis-generating findings.
BACKGROUND:Cardiac magnetic resonance (CMR) performed early after ST-segment elevation myocardial infarction (STEMI) can improve major adverse cardiac event (MACE) risk prediction. We aimed to create a simple clinical-CMR risk score for early MACE risk stratification in STEMI patients. METHODS:We performed a multicenter prospective registry of reperfused STEMI patients (n = 1118) in whom early (1-week) CMR-derived left ventricular ejection fraction (LVEF), infarct size and microvascular obstruction (MVO) were quantified. MACE was defined as a combined clinical endpoint of cardiovascular (CV) death, non-fatal myocardial infarction (NF-MI) or re-admission for acute decompensated heart failure (HF). RESULTS:During a median follow-up of 5.52 [2.63-7.44] years, 216 first MACE (58 CV deaths, 71 NF-MI and 87 HF) were registered. Mean age was 59.3 ± 12.3 years and most patients (82.8%) were male. Based on the four variables independently associated with MACE, we computed an 8-point risk score: time to reperfusion >4.15 h (1 point), GRACE risk score > 155 (3 points), CMR-LVEF <40% (3 points), and MVO >1.5 segments (1 point). This score permitted MACE risk stratification: MACE per 100 person-years was 1.96 in the low-risk category (0-2 points), 5.44 in the intermediate-risk category (3-5 points), and 19.7 in the high-risk category (6-8 points): p < 0.001 in multivariable Cox survival analysis. CONCLUSIONS:A novel risk score including clinical (time to reperfusion >4.15 h and GRACE risk score > 155) and CMR (LVEF <40% and MVO >1.5 segments) variables allows for simple and straightforward MACE risk stratification early after STEMI. External validation should confirm the applicability of the risk score.
Background: Coronary arteries supply oxygen and nutrients to the heart. We evaluated the dynamics of microscopic damage throughout the ischemia-reperfusion process in the wall of coronary arteries following myocardial infarction (MI). Methods: In a swine model of reperfused MI, animals were divided into one control and four MI groups: 90-min ischemia without reperfusion, or followed by one minute, one week or one month reperfusion. Left anterior descending (LAD; infarct-related artery) and control right coronary arteries (RCA) were isolated. Taking the balloon inflation region as a reference, we isolated the proximal and distal LAD areas, performing histological staining and immunohistochemistry. Results: Although mild changes in tunica intima were observed during ischemia, an almost complete absence of endothelium, and abnormal breaks in the internal elastic layer were found post-revascularization. In tunica media, increased thickness was observed soon after reperfusion, whereas larger thickness, disorganized muscle cell distribution and edema were found one week after reperfusion. This damage was more pronounced in distal rather than proximal LAD, whereas no changes were detected in RCA. In the tunica adventitia, vasa vasorum density decayed during ischemia in both LAD regions, but was restored after one month. Leukocyte adhesion to the artery was observed post-revascularization, developing into a massive presence in the three layers one week post-reperfusion. Conclusions: Ischemia-reperfusion can itself induce damage in the wall of the epicardial coronary artery, becoming more pronounced in the region distal to balloon inflation. Exploring these abnormalities will provide insight into the pathophysiology of coronary circulation and MI. (c) 2021 The Author(s). Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Aims The role of revascularization in chronic coronary syndrome (CCS) and the value of ischaemia vs. anatomy to guide decision-making are in constant debate. We explored the potential of a combined assessment of ischaemic burden by vasodilator stress cardiovascular magnetic resonance (CMR) and presence of multivessel disease by angiography to predict the effect of revascularization on all-cause mortality in CCS. Methods and results The study group comprised 1066 CCS patients submitted to vasodilator stress CMR pre-cardiac catheterization (mean age 66 +/- 11 years, 69% male). Stress CMR-derived ischaemic burden (extensive if >5 ischaemic segments) and presence of multivessel disease in angiography (two- or three-vessel or left main stem disease) were computed. The influence of revascularization on all-cause mortality was explored and adjusted hazard ratios (HRs) with the corresponding 95% confidence intervals were obtained. During a median 7.51-year follow-up, 557 (52%) CMR-related revascularizations and 308 (29%) deaths were documented. Revascularization exerted a neutral effect on all-cause mortality in the whole study group [HR 0.94 (0.74-1.19), P = 0.6], in patients without multivessel disease [n = 598, 56%, HR 1.12 (0.77-1.62), P = 0.6], and in those with multivessel disease without extensive ischaemic burden [n = 181, 17%, HR 1.66 (0.91-3.04), P = 0.1]. However, compared to non-revascularized patients, revascularization significantly reduced all-cause mortality in patients with simultaneous multivessel disease and extensive ischaemic burden (n = 287, 27%): 3.77 vs. 7.37 deaths per 100 person-years, HR 0.60 (0.40-0.90), P = 0.01. Conclusions In patients with CCS submitted to catheterization, evidence of simultaneous extensive CMR-related ischaemic burden and multivessel disease identifies the subset in whom revascularization can reduce all-cause mortality.
OBJECTIVES: This study explored the association of ischemic burden, as measured by vasodilator stress cardiovascular magnetic resonance (CMR), with all-cause mortality and the effect of revascularization on all-cause mortality in patients with stable ischemic heart disease (SIHD). Background: In patients with SIHD, the association of ischemic burden, derived from vasodilator stress CMR, with all-cause mortality and its role for decision-making is unclear. METHODS: The registry consisted of 6,389 consecutive patients (mean age: 65 +/- 12 years; 38% women) who underwent vasodilator stress CMR for known or suspected SIHD. The ischemic burden (at stress first-pass perfusion imaging) was computed (17-segment model). The effect of CMR-related revascularization (within the following 3 months) on all-cause mortality was retrospectively explored using the electronic regional health system registry. RESULTS: During a 5.75-year median follow-up, 717 (11%) deaths were documented. In multivariable analyses, more extensive ischemic burden (per 1-segment increase) was independently related to all-cause mortality (hazard ratio: 1.04; 95% confidence interval: 1.02 to 1.07; p < 0.001). In 1,032 1:1 matched patients using a limited number of variables (516 revascularized, 516 non-revascularized), revascularization within the following 3 months was associated with less all-cause mortality only in patients with extensive CMR-related ischemia (>5 segments, n = 432; 10% vs. 24%; p = 0.01). CONCLUSIONS: In a large retrospective registry of unselected patients with known or suspected SIHD who underwent vasodilator stress CMR, extensive ischemic burden was related to a higher risk of long-term, all-cause mortality. Revascularization was associated with a protective effect only in the restricted subset of patients with extensive CMR-related ischemia. Further research will be needed to confirm this hypothesis-generating finding. (C) 2020 by the American College of Cardiology Foundation.
Purpose In ST-segment elevation myocardial infarction (STEMI) patients, longitudinal strain (LS) in remote non-infarcted myocardium (RNM) has not yet been characterized by tissue tracking (TT) cardiovascular magnetic resonance (CMR). In STEMI patients, we aimed to characterize RNM-LS by TT-CMR and to assess both its dynamics and its structural and prognostic implications. Methods We recruited 271 patients with a first STEMI studied with TT-CMR 1 week after infarction. Of these patients, 145 underwent 1-week and 6-month TT-CMR and were used to characterize both the dynamics and the short-term and long-term structural implications of RNM-LS. Based on previously validated data, RNM areas were defined depending on the culprit coronary artery. Results Reduced RNM-LS at 1 week (n = 70, 48%) was associated with larger infarct size and more depressed left ventricular ejection fraction (LVEF) at both the 1-week and 6-month TT-CMR (p value < 0.001). Late normalization of RNM-LS was frequent (28/70, 40%) and independently related to late recovery of LVEF (p value = 0.002). Patients with reduced RNM-LS at 1-week TT-CMR had more major adverse cardiac events (death, heart failure or re-infarction) in both the 271 patients included in the study group (26% vs. 11%, p value = 0.002) and in an external validation cohort made up of 177 STEMI patients (57% vs. 13%, p value < 0.001). Conclusion After STEMI, reduced RNM-LS by TT-CMR is common and is associated with more severe short- and long-term structural damage. There is a beneficial tendency towards recovery of RNM-LS that parallels late recovery of LVEF. More events occur in patients with reduced RNM-LS.
Background Cardiac magnetic resonance (CMR) permits robust risk stratification of discharged ST-segment-elevation myocardial infarction patients, but its indiscriminate use in all cases is not feasible. We evaluated the utility of left ventricular ejection fraction (LVEF) by echocardiography for a selective use of CMR after ST-segment-elevation myocardial infarction. Methods Echocardiography and CMR were performed in 1119 patients discharged for ST-segment-elevation myocardial infarction included in a multicenter registry. The prognostic power of CMR beyond echocardiography-LVEF was assessed using adjusted C statistic, net reclassification improvement index, and integrated discrimination improvement index. Results During a 4.8-year median follow-up, 136 (12%) first major adverse cardiac events (MACE) occurred (47 cardiovascular deaths and 89 readmissions for acute heart failure). In the entire group, CMR-LVEF (but not echocardiography-LVEF) independently predicted MACE occurrence. The MACE rate significantly increased only in patients with CMR-LVEF<40% (≥50%: 7%, 40%-49%: 9%, <40%: 27%, P<0.001). Most patients displayed echocardiography-LVEF≥50% (629, 56%), and they had a low MACE rate (57/629, 9%). In patients with echocardiography-LVEF<50% (n=490, 44%), the MACE rate was also low in those with CMR-LVEF≥40% (24/278, 9%) but significantly increased in patients with CMR-LVEF<40% (55/212, 26%; P<0.001). Compared with echocardiography-LVEF, CMR-LVEF significantly improved MACE prediction in the group of patients with echocardiography-LVEF<50% (C statistic, 0.80 versus 0.72; net reclassification improvement index, 0.73; integrated discrimination improvement index, 0.10) but not in those with echocardiography-LVEF≥50% (C statistic 0.66 versus 0.66; net reclassification improvement index, 0.17; integrated discrimination improvement index, 0.01). Conclusions A straightforward strategy based on a selective use of CMR for risk prediction in ST-segment-elevation myocardial infarction patients with echocardiography-LVEF<50% can provide insights into patient care. The cost-effectiveness of this approach, as well as the direct implications in clinical management, should be further explored.
Purpose To characterize the incidence, outcomes, and predictors of left ventricular (LV) thrombus by using sequential cardiac magnetic resonance (MR) imaging after ST-segment-elevation myocardial infarction (STEMI). Materials and Methods Written informed consent was obtained from all patients, and the study protocol was approved by the committee on human research. In a cohort of 772 patients with STEMI, 392 (mean age, 58 years; range, 24-89 years) were retrospectively selected who were studied with cardiac MR imaging at 1 week and 6 months. Cardiac MR imaging guided the initiation and withdrawal of anticoagulants. Patients with LV thrombus at 6 months were restudied at 1 year. For predicting the occurrence of LV thrombus, a multiple regression model was applied. Results LV thrombus was detected in 27 of 392 patients (7%): 18 (5%) at 1 week and nine (2%) at 6 months. LV thrombus resolved in 22 of 25 patients (88%) restudied within the first year. During a mean follow-up of 181 weeks ± 168, patients with LV thrombus displayed a very low rate of stroke (0%), peripheral embolism (0%), and severe hemorrhage (n = 1, 3.7%). LV ejection fraction (LVEF) less than 50% (P < .001) and anterior infarction (P = .008) independently helped predict LV thrombus. The incidence of LV thrombus was as follows: (a) nonanterior infarction, LVEF 50% or greater (one of 135, 1%); (b) nonanterior infarction, LVEF less than 50% (one of 50, 2%); (c) anterior infarction, LVEF 50% or greater (two of 92, 2%); and (d) anterior infarction, LVEF less than 50% (23 of 115, 20%) (P < .001 for the trend). Conclusion Cardiac MR imaging contributes information for the diagnosis and therapy of LV thrombus after STEMI. Patients with simultaneous anterior infarction and LVEF less than 50% are at highest risk. © RSNA, 2017 Online supplemental material is available for this article.