In vivo effects of contrast media on coronary thrombolysis

AbstractObjectives. The aim of the present study was to evaluate the influence of radiographic contrast media (CM) on alteplase-induced coronary thrombolysis.Background. Contrast media inhibit fibrinolysis in vitro and interact with endothelial cells, platelets and the coagulation system. The in vivo effects of CM on thrombolysis are not known.Methods. Occlusive coronary artery thrombosis was induced in 4 groups of 10 dogs by the copper coil technique. After 70 min of occlusion the dogs were randomized to intracoronary injection of 2 ml kg−1of either saline, a low-osmolar ionic CM (ioxaglate), a low-osmolar nonionic CM (iohexol) or a high-osmolar ionic CM (amidotrizoate). Thrombolysis with alteplase and co-therapy with aspirin and heparin was initiated after 90 min of occlusion. The coronary artery flow was monitored with an electromagnetic flowmeter throughout the experiment.Results. Iohexol and amidotrizoate, but not ioxaglate, were associated with longer reperfusion delays (time to optimal reperfusion: 67 ± 48 min and 65 ± 49 min, respectively, vs. 21 ± 11 min after placebo; p < 0.05) and shorter periods of coronary perfusion (optimal perfusion time: 21 ± 26 min and 21 ± 28 min, respectively, vs. 58 ± 40 min after placebo; p < 0.05). No significant differences were observed between groups with regard to activated partial thromboplastin times, circulating thrombin-antithrombin III complex concentrations and fibrinogen.Conclusions. In this animal model administration of iohexol and amidotrizoate before thrombolysis significantly delayed reperfusion. This interaction should be considered in the design of clinical trials of thrombolytic therapy that evaluate coronary artery patency and in patients receiving local infusions of fibrinolytic agents

Higher myocardial strain rates duringisovolumic relaxation phase than duringejection characterize acutely ischemic myocardium

AbstractObjectivesThe aim of this study was to define an index that can differentiate normal from ischemic myocardial segments that exhibit postsystolic shortening (PSS).BackgroundIdentification of ischemia based on the reduction of regional systolic function is sometimes challenging because other factors such as normal nonuniformity in contraction between segments, tethering effect, pharmacologic agents, or alterations in loading conditions can also cause reduction in regional systolic deformation. The PSS (contraction after the end of systole) is a sensitive marker of ischemia; however, inconsistent patterns have also been observed in presumed normal myocardium.MethodsTwenty-eight open-chest pigs underwent echocardiographic study before and during acute myocardial ischemia induced by coronary artery occlusion. Ultrasound-derived myocardial longitudinal strain rates were calculated during systole (SSR), isovolumic relaxation (IVRSR), and rapid filling (ESR) phases in both ischemic and normal myocardium. Systolic strain (ϵsys) and postsystolic strain (ϵps) were calculated by integrating systolic and postsystolic strain rates, respectively.ResultsDuring ischemia, SSR, ESR, and ϵsys in ischemic segments were significantly lower (in magnitude) than in nonischemic segments or at baseline. However, some overlap occurred between ischemic and normal values for all three parameters. At baseline, 18 of 28 animals had negative IVRSR (i.e., PSS) in at least one segment. During coronary artery occlusion, IVRSR became negative and larger in magnitude than SSR in all ischemic segments. The IVRSR/SSR and ϵps best differentiated ischemic from nonischemic segments.ConclusionsIn the presence of reduced regional systolic deformation, a higher rate of PSS than systolic shortening identifies acutely ischemic myocardium

Intracardiac measurement of pre-ejection myocardial velocities estimates the transmural extent of viable myocardium early after reperfusion in acute myocardial infarction

AbstractOBJECTIVESWe hypothesized that wall motion velocity during pre-ejection is proportional to the regional content of viable myocardium after reperfusion for acute myocardial infarction (AMI).BACKGROUNDPre-ejection wall motion consists of short and fast inward and outward movement towards and away from the center of the left ventricle (LV) and is altered during regional ischemia. This short-lived event can be accurately quantified by Doppler myocardial imaging (DMI).METHODSFourteen open-chest pigs underwent 60 to 120 min of left anterior descending coronary artery occlusion followed by 30 min of reperfusion. The DMI data were collected using a phased-array intracardiac catheter (LV cavity) from ischemic and nonischemic myocardium encompassed within a plane passing through two epicardial bead markers. Peak tissue velocities during isovolumic contraction (IVC) (peak positive and peak negative), ejection (S) and early filling (E) were measured. The cardiac specimen was sliced through the epicardial markers in a plane approximating the ultrasound imaging plane. The transmural extent of necrosis (TEN) (%) was measured by triphenyltetrazolium chloride staining.RESULTSDuring ischemia, positive IVC velocity was zero in ischemic walls with TEN >20%. At reperfusion, positive IVC velocity correlated better with TEN (r = −0.94, p < 0.0001) than it did S (r = −0.70, p < 0.01) and E (r = −0.81, p < 0.01). Differential IVC (the difference between peak positive and peak negative velocity) highly correlated with TEN, during ischemia (r = −0.78, p < 0.001) and during reperfusion (r = −0.93, p < 0.0001).CONCLUSIONSPre-ejection tissue velocity, as measured by intracardiac ultrasound, allows rapid estimation of the transmural extent of viable myocardium after reperfusion for AMI

Strain echocardiography tracks dobutamine-induced decrease in regional myocardial perfusion in nonocclusive coronary stenosis

ObjectivesThis study was designed to determine whether strain echocardiography parameters reflect changes in regional myocardial perfusion during dobutamine stress.BackgroundStrain echocardiography depicts regional myocardial mechanical activity. Ischemia has been shown to reduce systolic strain rate (sSR) and prolong the time to regional lengthening (TRL). In an experimental model, we tested whether sSR and TRLtracked dobutamine-induced changes in regional myocardial perfusion (regional myocardial blood flow [RMBF]), as measured by colored microspheres.MethodsWe used a closed-chest pig model of nonocclusive coronary stenosis (n = 14) created by inflating an angioplasty balloon in the proximal left anterior descending artery. Invasive hemodynamics, RMBF, and strain parameters were measured at baseline and peak dobutamine stimulation before and during the coronary stenosis. We compared segments with reduced RMBF versus those with preserved RMBF at peak dobutamine stimulation.ResultsPeak sSR correlated with RMBF (r = 0.70). In the absence of coronary stenosis, dobutamine stimulation caused a significant increase in RMBF and sSR and a decrease in TRL. This response was blunted during coronary stenosis. Using the “best cutoff” method, the sensitivity and specificity for prediction of reduced RMBF (ischemia) was 81% and 91% for sSR and 65% and 91% for TRL, respectively. These changes occurred in the absence of any change in global systolic and diastolic function (dP/dTmax, dP/dTmin, and tau).ConclusionsNovel strain parameters that depict regional myocardial mechanics are able to predict changes in RMBF during dobutamine stress. Quantitative strain parameters may complement current echocardiographic techniques for ischemia detection and potentially improve the accuracy and reproducibility of stress echocardiography

Alterations in Cardiac Deformation, Timing of Contraction and Relaxation, and Early Myocardial Fibrosis Accompany the Apparent Recovery of Acute Stress-Induced (Takotsubo) Cardiomyopathy : An End to the Concept of Transience

This work was supported by grants from Tenovus Scotland and the British Heart Foundation (to Dr. Dawson, G13/10 and PG/15/108/31928, respectively). Dr. Dawson has a research agreement with Philips Healthcare and holds a material transfer agreement with AMAG Pharmaceuticals.Peer reviewedPostprin

Report from the Annual Conference of the British Society of Echocardiography, November 2016, Queen Elizabeth II Conference Centre, London.

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