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Introduction: Pulmonary embolism, an emergency that can have fatal consequences, can be presented with a common symptom that can be missed, such as syncope.Case presentation: We present a case of a young, low-risk male who presented with attacks of syncope and dyspnea followed by massive pulmonary embolism. We also review the pathophysiology of syncope in pulmonary embolism cases and strategy of how to work up with similar cases.Conclusion: Pulmonary embolism should be considered and excluded in every case of recurrent attacks of syncope.

We assessed the very long-term follow-up of a large cohort of unselected patients treated with coronary rotational atherectomy (RA). All 143 patients who underwent RA at our institution from 2000 to 2013 and with complete baseline and follow-up information were analyzed in a retrospective manner. Major adverse cardiac events (MACE) were defined as the composite of target vessel revascularization (TVR), acute myocardial infarction, and all-cause mortality. The mean follow-up was 8.2 years. The 10-year cumulative incidence of MACE for all patients was 57.9% (standard error [SE]: 5.0%). When comparing patients who received a drug-eluting stent (DES; n = 68) versus patients who did not (balloon only, bare-metal stent, or none of the aforementioned; n = 75), the RA + DES demonstrated very long-term MACE of 49.2% (SE: 7.5%) versus 62.7% (SE: 6.1%), P = .160 with TVR as the most discriminating factor, 10.7% (SE: 4.0%) versus 29.2% (SE: 6.0%), P = .016. Our results point to RA having reasonable long-term clinical results, especially in combined treatment with DES. To date, our study has the longest follow-up after RA.

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Background:Ischemic heart diseaseis one of the heaviest health-related burdens worldwide.We aimed to identify the common hub mRNA and pathways that are involved in pathological progression of ischemic cardiomyopathy(ICM). Methods:To explore potential differentially expressed genes (DEGs) of all ischemic heart disease stages, we used chipster and GEO2R tools to analyze of retrieved eight high throughput RNA datasets obtained from GEO database. Gene Ontology functional annotation and Pathways enrichment analyses were used to obtain the common functional enriched DEGs which were visualized in protein–protein interactions (PPI) network to explore the hub mRNA according to the interaction scores. Validation qRT-PCR was carried out for blood and cardiac biopsies compared with controls to validate the determined four hub mRNAs and subsequently reviewed inside comprehensive published meta-analysis database. The validated mRNAs were visualized in two interaction modules. Finally screening of approved drugs was applied. Results: 15 common DEGs with p value ≤ 0.01 were identified and carbohydrate &amino acids metabolism and inflammatory responses were significantly enriched. STAT3, CEBPD, GLUL and CD163 were hub enriched mRNAs with interaction score ≥ 0.50. Our qRT-PCR analysis showed increased expression of STAT3 over all patients groups and CD163 mainly in cardiac samples with remarked ascending manner. Interaction modules showed co-regulators supporting high STAT3-CD163 connectivity providing potential role of STAT3-CD163 crosstalk mediated inflammatory responses in ICM progression. We determined two reported drugs targeting STAT3. Conclusion:Post analysis of the used GEO datasets and qRT-PCR data pointed that STAT3-CD163 crosstalk was potential biomarkers for ICM progression. Clinical trial registration: www.clinicaltrials.gov, Identifier: NCT05508269