Search

International audience; Primary percutaneous coronary intervention (PCI) is the best available reperfusion strategy for acute ST-segment elevation myocardial infarction (STEMI), with nearly 95% of occluded coronary vessels being reopened in this setting. Despite re-establishing epicardial coronary vessel patency, primary PCI may fail to restore optimal myocardial reperfusion within the myocardial tissue, a failure at the microvascular level known as no-reflow (NR). NR has been reported to occur in up to 60% of STEMI patients with optimal coronary vessel reperfusion. When it does occur, it significantly attenuates the beneficial effect of reperfusion therapy, leading to poor outcomes. The pathophysiology of NR is complex and incompletely understood. Many phenomena are known to contribute to NR, including leukocyte infiltration, vasoconstriction, activation of inflammatory pathways and cellular oedema. Vascular damage and haemorrhage may also play important roles in the establishment of NR. In this review, we describe the pathophysiological mechanisms of NR and the tools available for diagnosing it. We also describe the microvasculature and the endothelial mechanisms involved in NR, which may provide relevant therapeutic targets for reducing NR and improving the prognosis for patients.

SummaryHeart involvement, including primary myocardial involvement, is very common in systemic sclerosis. There is strong evidence that primary myocardial involvement is related to repeat focal ischaemic injury causing subsequent irreversible myocardial fibrosis. Clinically evident cardiac involvement is recognized to be a poor prognostic factor; thus preclinical identification is highly encouraged. The severity of heart involvement has been confirmed recently. Echocardiography, including pulsed tissue Doppler echocardiography, is the cornerstone of routine heart assessment. Myocardial perfusion may be assessed by single photon emission computed tomography. If available, cardiac magnetic resonance imaging should be considered as it allows simultaneous measurement of ventricular volumes and function and myocardial perfusion, and assessment of possible inflammation and/or fibrosis. Biological variables, such as B-type natriuretic peptides, are highly relevant, valuable markers of global heart involvement in systemic sclerosis and should be considered for screening of patients and/or research purposes.

SummaryTissue Doppler imaging and strain rate imaging are quantitative methods for assessing myocardial function and have been shown to overcome the limitations of current ultrasound methods in assessing the complex changes in regional myocardial function that occur in differing ischemic substrates. Tissue Doppler imaging (TDI) measures in real time the myocardial velocity gradient which is an index of myocardial deformation. Strain and strain rate (SR) imaging has been shown to be a sensitive technique for quantifying regional myocardial deformation. Strain rate is less load-dependent that strain and provides therefore a better measure of contractility.In the setting of ischemia, experimental studies have shown that strain imaging was an accurate method for quantitative evaluation of regional myocardial function and may yield important physiological data. In myocardial infarction, transmural extension of scar distribution in the infarct zone is proportionally related to the reduction in systolic function measured by the radial transmural velocity gradient or by strain rate imaging. Measurement of both systolic and post-systolic deformation both at rest and during a graded dobutamine infusion may help to distinguish between transmural and non transmural infarcts.In conclusion, strain imaging has the ability to evaluate of regional myocardial function. Strain rate has not replaced conventional grey-scale imaging in the assessment of regional left ventricular function and the implement of these new indices in the routine clinical practice will need additional clinical and large-scale studies.