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Abstract

The efficacy of cardioprotective strategies can be quantified by myocardial salvage as an indicator of therapeutic benefit. Salvage is calculated as the difference between the area at risk (AAR) and the final infarct size (FIS). AAR has been quantified by angiographic assessment followed by quantification of FIS by biochemical ischaemic markers or imaging modalities such as cardiovascular magnetic resonance (CMR). Angiographical methods may overestimate AAR and since methodological differences may exist between different modalities, the use of different modalities for estimating AAR and FIS may not be recommended. 99m Technetium (Tc)-Sestamibi single-photon emission tomography (SPECT) allows quantification of AAR and FIS by tracer injection prior to revascularization and after 1 month, respectively. SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomized clinical trials. However, SPECT is logistically challenging, expensive, and includes radiation exposure. More recently, a large number of studies have suggested that CMR can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement. The T1- and T2-weighted CMR approaches for quantification of AAR utilize non-contrast, early and late gadolinium enhancement techniques. The technical progress, high spatial resolution and the potential for retrospective quantification of the AAR makes CMR the most appropriate technique for assessment of myocardial salvage. However, the optimum CMR technique for assessment of myocardial AAR remains to be defined. Consequently, we recommend a comprehensive CMR protocol to ensure reliable assessment of myocardial salvage.

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Salvage of threatened myocardium is the principal mechanism by which patients with acute myocardial infarction (AMI) benefit from reperfusion. The combination of interventional and medical treatment has reduced mortality and morbidity significantly. Consequently, large patient numbers are required in clinical trials that aim at demonstrating improved survival of a new treatment. To diminish the need for large population sizes, numerous trials have used surrogate endpoints, including imaging measures of infarct size after coronary revascularization and indirect estimates of tissue damage by release of biomarkers, resolution of ST-segment elevation and myocardial blush grade. 1 , 2 Although these endpoints have predictive power in large cohorts, the usefulness in the individual patient and in small-sized study populations is moderate. 3 More recent clinical studies have used FIS and myocardial salvage as the primary endpoint ( Table 1 ). 4–7 Techniques that allow quantification of myocardial salvage provide advantages compared with those measuring only FIS: (i) quantification of salvage rather than FIS eliminates inter-individual variability and reduces requirement to the study population size, (ii) they permit proof-of-concept studies to test the potential efficacy of new therapeutic approaches in smaller study groups, and importantly (iii) they may provide further insight into the pathophysiology of ischaemia-reperfusion injury. The electrocardiogram may be used to estimate area at risk (AAR), but not FIS. 8 Indirect measures of salvage can be calculated from angiographic estimates of AAR combined with estimates of FIS by imaging techniques or biochemical markers. Echocardiography is the preferred clinical method for evaluation of left ventricular (LV) function in patients with AMI. However, there are currently no specific echocardiographic measures of myocardial salvage. 99m Technetium (Tc)-Sestamibi single-photon emission tomography (SPECT) and cardiovascular magnetic resonance (CMR) provide the assessment of myocardial salvage, using paired quantification of AAR and FIS either from two separate studies before and after revascularization, or retrospectively in one step when the patient has been treated and stabilized. The aim of the present review is to provide an overview of the current methods used for quantification of myocardial salvage in preclinical studies and clinical trials assessing the efficacy of reperfusion therapy and cardioprotection in AMI.

The effect of the fluoroquinolones on insulin secretion has been studied, and the results suggest that these antibiotics cause hypoglycemia by increasing insulin release via blockade of adenosine triphosphate-sensitive K + channels in the β cells of the pancreas [ 30 , 31 ]. This effect may not be clinically significant in all patients because of physiologic mechanisms that regulate blood glucose levels. In contrast, the mechanism of hyperglycemia is not clear. One contributing factor may be overexposure (eg, failure to adjust the dose in patients with renal insufficiency) [ 32 ]. The results of our study and of others [ 12 , 15 , 16 , 20 , 21 ], as well as this potentially common mechanism for hypoglycemia, suggest the need for caution when using certain fluoroquinolones, because the odds of hypo- and hyperglycemia appear to vary among the agents [ 33 ]. This is not unusual; differences in risk have been reported for other adverse effects with this class of antibiotics [ 34 ].

Our results are generally consistent with those presented in the literature. In a retrospective medical-record review of dysglycemia in hospitalized patients receiving gatifloxacin, levofloxacin, ciprofloxacin, or ceftriaxone, dysglycemic events were more likely to occur in patients receiving gatifloxacin (relative risk, 3.29; 95% CI, 2.33–4.65) or levofloxacin (relative risk, 1.55; 95% CI, 1.29–1.88) versus ceftriaxone [ 20 ]. There was no difference in the risk of dysglycemia between gatifloxacin and levofloxacin (P=.8). However, hypo- and hyperglycemic events were combined in this study. None of the patients who received ciprofloxacin experienced a dysglycemic event. In a nested case-control study of hospitalized patients who received gatifloxacin or levofloxacin, the odds of hypoglycemia were greater with gatifloxacin versus levofloxacin (OR, 2.81; 95% CI, 1.02–7.70) [ 12 ]. No comparator antibiotic was included in the study, so the possibility of a fluoroquinolone class effect could not be assessed. In another study of elderly inpatients who received gatifloxacin or levofloxacin, gatifloxacin was independently associated with hypoglycemia (OR, 2.4; 95% CI, 1.1–5.6) and hyperglycemia (OR, 2.5; 95% CI, 1.6–3.9) versus levofloxacin [ 21 ]. Again, a nonfluoroquinolone antibiotic was not included in the study.

Dysglycemic events have also been evaluated among outpatients receiving fluoroquinolones. In a smaller, regional database review of the effect of fluoroquinolones on glucose metabolism among veterans with an outpatient or discharge prescription for any of these antibiotics, Coblio et al [ 15 ] state that gatifloxacin was no more likely to cause hypo- or hyperglycemia than levofloxacin or ciprofloxacin among patients with or without diabetes, but they did not report statistical significance. In addition, no comparator was included, so the possibility of a class effect could not be assessed. In a nested case-control study of outpatient fluoroquinolone therapy and dysglycemia requiring hospitalization, gatifloxacin (OR, 4.3; 95% CI, 2.9–6.3) and levofloxacin (OR, 1.5; 95% CI, 1.2–2.0) were associated with an increased risk of hypoglycemia versus macrolides, but ciprofloxacin and moxifloxacin were not [ 16 ]. Compared with macrolide antibiotics, only gatifloxacin was associated with an increased risk of hyperglycemia (OR, 16.7; 95% CI, 10.4–26.8). The authors' findings were similar when their results were stratified by the presence or absence of diabetes. In our study, the small number of events in patients without diabetes (despite our large sample) combined with low ORs and lack of statistical significance suggest that clinical focus regarding risk with the remaining fluoroquinolones should be on those with diabetes.

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