After progressively receding for decades, cardiovascular mortality due to coronary artery disease has recently increased, and the associated healthcare costs are projected to double by 2030. While the 2019 European Society of Cardiology guidelines for chronic coronary syndromes recommend non-invasive cardiac imaging for patients with suspected coronary artery disease, the impact of non-invasive imaging strategies to guide initial coronary revascularization and improve long-term outcomes is still under debate. Recently, the ISCHEMIA trial has highlighted the fundamental role of optimized medical therapy and the lack of overall benefit of early invasive strategies at a median follow-up of 3.2 years. However, sub-group analyses excluding procedural infarctions with longer follow-ups of up to 5 years have suggested that patients undergoing revascularization had better outcomes than those receiving medical therapy alone. A recent sub-study of ISCHEMIA in patients with heart failure or reduced left ventricular ejection fraction (LVEF <45%) indicated that revascularization improved clinical outcomes compared to medical therapy alone. Furthermore, other large observational studies have suggested a favorable prognostic impact of coronary revascularization in patients with severe inducible ischemia assessed by stress cardiovascular magnetic resonance (CMR). Indeed, some data suggest that stress CMR-guided revascularization assessing the extent of the ischemia could be useful in identifying patients who would most benefit from invasive procedures such as myocardial revascularization. Interestingly, the MR-INFORM trial has recently shown that a first-line stress CMR-based non-invasive assessment was non-inferior in terms of outcomes, with a lower incidence of coronary revascularization compared to an initial invasive approach guided by fractional flow reserve in patients with stable angina. In the present review, we will discuss the current state-of-the-art data on the prognostic value of stress CMR assessment of myocardial ischemia in light of the ISCHEMIA trial results, highlighting meaningful sub-analyses, and still unanswered opportunities of this pivotal study. We will also review the available evidence for the potential clinical application of quantifying the extent of ischemia to stratify cardiovascular risk and to best guide invasive and non-invasive treatment strategies.
SUMMARY INTRODUCTION In acute myocardial infarction (AMI), each 18 mg/dl (1 mmol/L) increment is associated with a 3% increase in mortality rates. All strategies applied for reducing blood glucose to this date, however, have not presented encouraging results. METHODOLOGY We searched the Medline (PubMed) and Cochrane Library databases for randomized clinical trials (RCTs) from 1995 to 2017 that used the intensive strategy or GIK therapy for blood glucose control during the acute stage of the AMI. We included eight studies. In order to identify the effects of GIK or insulin therapy, we calculated a overall risk ratio (RR) with meta-analysis of fixed and random effects models. A two-tail p-value of < 0.05 was considered statistically significant. RESULTS A total of 28,151 patients were included: 1,379 intensively treated with insulin, 13,031 in GIK group, and 13,741 in the control group. The total mortality was 10.5% (n=2,961) and the RR of 1.03 [95%CI 0.96–1.10]; I2 = 31%; p = 0.41 for the combined intensive insulin plus GIK groups in comparison with the control group. In meta-regression analyses, intense reductions in blood glucose (> 36 mg/dL) in relation to the estimated average blood glucose (estimated by HbA1c) were associated with higher mortality, whereas lower reductions in blood glucose (< 36 mg/dL) were not associated with mortality. The lowering of blood glucose in the acute phase of MI compared with the average blood glucose was more effective around 18 mg/dL. CONCLUSION This meta-analysis suggests that there may be a tenuous line between the effectiveness and safety of reducing blood glucose in the acute phase of MI. The targets must not exceed a reduction greater than 36 mg/dL in relation to estimated average blood glucose.
Background An abnormal increase of cardiomyocyte mass of the left ventricle is observed in physiological and pathological phenotypes of hypertrophy. Aims To apply CMR tissue characterization using native T1/T2 and post-contrast T1 mapping and identify tissue phenotypes corresponding to physiological and pathological hypertrophy, in athletes and heart failure (HF), respectively. Methods/Results 187 individuals were prospectively enrolled, in 4 groups: Athletes (n=56, 32±13 years), HF with and without preserved ejection fraction (HFpEF: n=49, 62±12 years; HFrEF: n=49, 54±16 years, H2FpEF-score: 4.8 [3–9]), and healthy controls (n=33, 41±13.7 years). All participants underwent cardiopulmonary exercise testing and a multiparametric CMR study to assess morphology/function, T2, native T1, extracellular volume fraction (ECV), and intracellular lifetime of water (a marker of cardiomyocyte diameter). As expected, LVEF varied significantly among groups (Athletes: 64.7±6.1%, HFpEF: 59.3±10.7%, HFrEF: 29.4±8.5%, and controls: 65.4±4.3%, p<0.001) and was markedly reduced in HFrEF. Both LV mass index (Athletes: 64.1±15.8 g/m2, HFpEF: 62.3±24 g/m2, HFrEF: 79.5±36.7 g/m2, and controls: 42±9.2 g/m2, p<0.001) and cardiomyocyte mass index (calculated as (1 − ECV) x LV mass/BSA) (Athletes: 47.9±13.1 g/m2, HFpEF: 42.2±17.2 g/m2, HFrEF: 55.69±24.70 g/m2, and controls: 30.7±6.9 g/m2, p<0.001, Fig. 1A) were elevated in athletes and HF, compared to controls. Athletes and HFpEF patients showed concentric LV remodeling, while the eccentric LV remodeling was observed in HFrEF (Fig. 1B). In the HF groups NT-proBNP was elevated (Athletes: 34.6±16.8 ng/dL, HFpEF: 473.2±700.1 ng/dL, HFrEF: 1,365.3±1,772 ng/dL, and controls: 34.3±29 ng/dL, p<0.005), and adjusted maximum oxygen consumption was markedly reduced (Athletes: 49.4±9.3 mL/kg/min, HFpEF: 18.3±5.5 mL/kg/min, HFrEF: 17.1±4.2 mL/kg/min, and controls: 30.3±10.2 mL/kg/min, p<0.005). ECV was larger in both HF groups (athletes: 0.27±0.04, HFpEF: 0.31±0.05, HFrEF: 0.32±0.04, and controls: 0.26±0.02, p<0.001). The intracellular lifetime of water was longer among athletes compared to controls and shorter in HFrEF compared to HFpEF (Athletes: 0.17±0.07, HFpEF: 0.15±0.05, HFrEF: 0.13±0.05, and controls: 0.14±0.05, p<0.001). Native T1 was reduced in athletes compared to controls and elevated in the HF groups (Athletes: 1,173.4±63.2 ms, HFpEF: 1,262.8±62.4 ms, HFrEF: 1,275.1±59.9 ms, and controls: 1,212.78±76.01 ms, p<0.001). Lastly, the an increased T2 was indicative of edema in HF patients (Fig. 2). Conclusions In a prospective observational study with CMR T1/T2 mapping, physiological hypertrophy is characterized by increased cardiomyocyte diameter, normal ECV, and a decrease in native T1, due to the larger cardiomyocyte volume. In contrast, with pathological hypertrophy in HF, is associated with an increased and an above-normal native T1. Cardiomyocyte diameter appears reduced in HFrEF compared to HFpEF, reflecting the transition to an eccentric LV shape. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The São Paulo Research Foundation
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