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LV Function Deteriorates in Non-STEMI Patients Awaiting Cardiac Catheterization
Abstract & Commentary
By Andrew J. Boyle, MBBS, PhD
Source: Grenne B, et al. Changes of myocardial function in patients with non-ST-elevation acute coronary syndrome awaiting coronary angiography. Am J Cardiol. 2010;105:1212-1218.
The optimal timing of cardiac catheterization for patients suffering non-ST segment elevation myocardial infarction (nonSTEMI) remains a subject of debate. Research on early vs. delayed cardiac catheterization has focused on event rates (death, myocardial infarction [MI], and revascularization), but little is known about the effect of waiting for cardiac catheterization in left ventricular (LV) systolic function. Accordingly, Grenne and colleagues studied patients presenting to their center in Norway, with chest pain suggestive of nonSTEMI, and performed echocardiography at admission, immediately prior to cardiac catheterization and after revascularization. Global and regional myocardial function was measured as longitudinal and circumferential strain using speckle-tracking echocardiography.
They prospectively recruited 102 patients, and gave retrospective diagnoses after cardiac catheterization and cardiac enzyme results were known. Patients were divided into nonSTEMI (n = 56), unstable angina pectoris (UAP) (n = 23), and non-coronary chest pain (NCCP) (n = 23). Patients were excluded if they had severe valvular disease, previous heart surgery or bundle branch block, significant arrhythmia, reduced life expectancy, or very early, planned cardiac catheterization (< 10 hours). Echo was performed in parasternal views for circumferential strain and apical views for longitudinal strain. Using the 16-segment model, global strain was calculated by averaging all segmental peak-systolic strain values. Regional strain was calculated for the territory of each coronary artery, and the culprit vessel was then identified on coronary angiography.
Results: Mean time from admission to coronary angiography was 32 hours in all groups. Patients experiencing nonSTEMI were older (67 ± 14 years) than those suffering UAP or NCCP (58 ± 11 and 56 ± 10 years, respectively), and were less likely to have had previous percutaneous coronary intervention (PCI) (4% vs. 30% vs. 26%; p < 0.05). Medication usage was similar, with the exception that the NCCP group had lower statin use at the time of cardiac catheterization (100% vs. 100% vs. 74%; p < 0.05).
At admission, non-STEMI patients had worse longitudinal and circumferential strain, and patients with UAP had worse longitudinal strain than patients with NCCP (p < 0.05). In the non-STEMI patients, global LV function deteriorated in the 32 hours between admission and cardiac catheterization (p < 0.001), whereas there was no change in the UAP or NCCP groups. This was demonstrated by an increase in the global longitudinal strain in the non-STEMI patients, but there was no change in the circumferential strain. The change in global strain was driven purely by a worsening in the culprit artery territory, as there was no change in the strain in the remote region. Of note, the LV ejection fraction (EF) in the non-STEMI group was 53% ± 6% at admission and 51% ± 7% at cardiac catheterization, but this change did not reach statistical significance. There was no change in LVEF in the other groups.
The authors then separated the non-STEMI group further according to whether the culprit artery was completely occluded (n = 16) or nonoccluded (n = 40). Those with occluded culprit arteries had deterioration in both longitudinal and circumferential strain from admission to cardiac catheterization (p ≤ 0.01), and those with non-occluded arteries had deterioration in only the longitudinal strain during that time (p < 0.001). The authors offer an explanation for this. The predominance of longitudinal fibers in the subendocardial layer may be the reason that both occluded and non-occluded arteries result in ischemic deterioration in function here, because ischemia first affects subendocardial tissue. Thus, both complete and incomplete occlusion may render the subendocardium ischemic. With the majority of circumferential fibers being in the midwall of the LV, only the occluded artery patients experienced deterioration in circumferential strain, because only the patients with occluded arteries had transmural ischemia. This would seem to be a plausible explanation.
Follow-up of non-STEMI patients revealed that regional and global strain improved in those patients without occlusion who were revascularized, either by PCI or coronary artery bypass grafting. However, there was no benefit in those with an occluded artery. The authors conclude that myocardial function deteriorates in patients with nonSTEMIs awaiting coronary angiography, that patients with acute coronary occlusion have the most pronounced deterioration, and that this subgroup shows no recovery of function after revascularization.
Using a sensitive method to serially assess regional cardiac function, Grenne et al show us that there is regional deterioration in function in patients with nonSTEMI and a non-occluded artery over the first 32 hours in hospital. This corresponded to an overall decrease in global LV strain but not a significant decrement in LVEF. Importantly, this deterioration in cardiac function was reversible after revascularization. Patients with nonSTEMI and complete occlusion of the infarct artery also suffered deterioration in LV function in the first 32 hours in hospital, but this did not resolve after revascularization. It should be noted that this subgroup of patients was small (n = 16). Importantly, there was no deterioration in function in the absence of biomarkers of myocardial necrosis. It is noteworthy that the authors have not tested whether earlier intervention may prevent this deterioration in LV function. This must be tested in future prospective studies.