Background
Ectatic coronary segments are nidi for thrombus formation due to altered flow dynamics and stasis—an important component of Virchow’s triad. Ectasia accompanied by an adjacent coronary stenosis with or without a plaque event can lead to acute myocardial infarctions complicated by huge thrombus burden.
Case summary
Here, we present a case of a young male with acute inferior wall myocardial infarction complicated by Type IV coronary artery ectasia of the right coronary artery and huge thrombus burden that was refractory to conventional methods of thrombus management like thrombo-suction and intracoronary cocktails including tenecteplase. After a stormy course of transient complete heart block and recurrent ventricular tachycardia, the thrombus was successfully extracted using a stent retriever to achieve thrombolysis in myocardial infarction (TIMI) II plus flow distally. The lesion just distal to the ectasia was stented 24 h later to achieve TIMI III flow and the patient had an uneventful recovery subsequently.
Discussion
Angiographically visible thrombus that is refractory to intracoronary medications and aspiration thrombectomy can be successfully managed using a stent retriever.
Fluorescence lifetime imaging microscopy (FLIM) evaluates the metabolic state of tissue based on reduced nicotinamide adenine dinucleotide (NAD(P)H) and flavin adenine dinucleotide (FAD). Fluorescence lifetime imaging ophthalmoscopy (FLIO) can image the fundus of the eyes, but cannot detect NAD(P)H. We used multiphoton FLIM to study the metabolic state of the retina in fixed eyes of wild-type mice C57BL6/J. We sectioned the eye using a polyacrylamide gel-embedding technique and estimated the percentage of bound NAD(P)H. We found that oxidative phosphorylation was the predominant metabolic state, particularly in the inner retina, when a fixed retina was used. We also demonstrated the feasibility of FAD imaging of the retina. In addition, we demonstrated that autofluorescence and various FLIM channels, such as hemoglobin, melanin and collagen, can be used to evaluate the structure of the retina and other parts of the eye without any special staining.
Human studies have established that short periods of dark adaptation can induce outer retinal thinning and various band intensity changes that can be detected with Optical Coherence Tomography (OCT). Similar findings were observed in mice, including a positive correlation between the degree of outer retinal changes and dark adaptation duration. We decided to assess potential retinal structural changes following prolonged dark adaptation in humans. 40 healthy subjects without any ocular diseases participated in this study. For each subject, one eye was covered for dark adaptation for four hours, and the other eye was left uncovered as a control. Before and after the dark adaptation period, both eyes were assessed with OCT. Using the Heidelberg Spectralis system, basic statistical functions, and qualitative and quantitative analysis, we were able to compare retinal layer thicknesses and band intensities between covered (dark adapted) versus uncovered (control) eyes. Prolonged dark adaptation did not induce any significant thickness, volume, or intensity changes in the outer retina or in the inner or overall retina. These observations thus alter our current understanding of the mechanisms underlying dark adaptation’s neuroprotective effects in preventing blindness and require further study.
Introduction: Here, we present a case of macular hole (MH) reopening after an initial successful closure with an inverted internal limiting membrane (ILM) flap procedure.
Case Report: The patient was a 72-year-old Hispanic male who presented with decreased vision in the right eye who was found to have a 431 μm, full-thickness macular hole. The patient underwent three separate 25-gauge pars plana vitrectomies to correct the macular hole. The first involved an inverted ILM flap technique, the second one removal of the flap and the third one subretinal injection of balanced salt solution (BSS).
Conclusion: The failure of the inverted ILM flap, we believe, was primarily due to the inferiorly attached flap being pulled down by surface tension of the rising fluid level.
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