Spontaneous coronary artery dissection (SCAD) and takotsubo cardiomyopathy (TCM) - A potential association.

Background: Spontaneous coronary artery dissection and takotsubo cardiomyopathy are increasingly recognized in the last two decades. Case reports have shown both entities can present concomitantly - however, little is known about their association. Methods: In this retrospective study we aimed to explore a potential association between SCAD and TCM using the Nationwide Inpatient Sample. The odds of having TCM among patients with SCAD compared with those who did not have SCAD were calculated as an odds ratio. Conversely, the odds of having SCAD among patients with TCM compared with those who did not have TCM were also calculated. The primary outcome was the odds of TCM among patients with a primary diagnosis of SCAD and vice versa. The secondary endpoint was the odds of in-hospital mortality among patients with SCAD, and/or TCM. Results: Hospitalized patients who had SCAD were 7.12 (95 % CI: 6.28-8.08) times more likely to also have TCM than those who did not have SCAD (p < 0.0001).), while patients with TCM were 6.91 (95 % CI: 6.07-7.85) times more likely to have SCAD compared to those who didn't have TCM adjusted for age, gender, race, hypertension, hyperlipidemia, and diabetes mellitus (p < 0.0001). Conclusion: This data indicate that patients with either SCAD or TCM are seven times more likely to be diagnosed concomitantly with both, compared to the patients without either diagnosis [after adjusting for age, gender, race, hypertension, hyperlipidemia, and diabetes mellitus]. Our data are consistent with the growing body of evidence supporting an association between SCAD and TCM and raise the question of a common pathophysiologic mechanism.

Histopathologic Characterization of Chronic Total Occlusions by Directional Atherectomy: The HIPACT Study.

BACKGROUND: Chronic total occlusions (CTOs) and long lesions have been associated with higher reocclusion rates in femoropopliteal arteries and increased need for revascularization. While several studies have analyzed atherectomy samples, no study to date has correlated the tissue characteristics of CTOs with clinical outcomes. This pilot study assessed lesions in order to predict clinical outcomes based on lesion characteristics. METHODS: Patients presenting with femoropopliteal (FP) CTO lesions, including in-stent restenosis and de novo lesions, were enrolled in a prospective, observational study. With patient consent, CTOs were crossed using a crossing catheter guided by optical coherence tomography (OCT) imaging. Atherectomy was performed with a directional atherectomy device and tissue samples were collected and subjected to histopathological analysis for the presence of adventitial tissue and thrombus, and the amounts of hypercellular cells, fibrocellular material, fibrous tissue, and lipid-rich tissue in the excised tissue were measured. The compiled data were correlated with clinical outcomes, as recorded at each patient's clinical follow-up visit. RESULTS: All CTO lesions (n = 19) were successfully crossed, with no dissections or perforations. Adventitial tissue was found in excised tissue from all 19 lesions (up to 57% of total lesion area), and thrombus was found in 15 lesions (up to 34% of total lesion area). The amount of hypercellular cells, fibrocellular material, fibrous tissue, and lipid-rich tissue present in the excised tissue did not correlate with the incidence of target-lesion revascularization (TLR). At 6-month follow-up exam, 79% of the treated lesions had TLR. Risk of TLR was assessed based on weighted risk of each variable; the results determined that occurrence of TLR was associated with elevated levels of adventitia and thrombus in the lesions and with lesions >15 cm in length. There was a significant correlation (P<.05) between TLR and the lesion characterization as set forth in the present study. CONCLUSIONS: Pairing the histological analysis, including content of adventitia and thrombus, with lesion length and binary clinical outcomes enabled the predictive incidence of TLR in this pilot study. Further work needs to be conducted to validate these findings in larger studies.

Race and gender variation in response to evoked inflammation.

BACKGROUND: Race- and gender-variation in innate immunity may contribute to demographic differences in inflammatory and cardiometabolic disease; yet their influence on dynamic responses during inflammatory stress is poorly understood. Our objective was to examine race and gender influence on the response to experimental endotoxemia. METHODS: The Genetics of Evoked Responses to Niacin and Endotoxemia (GENE) study was designed to investigate regulation of inflammatory and metabolic responses during low-grade endotoxemia (LPS 1 ng/kg intravenously) in healthy individuals (median age 24, IQR=7) of European (EA; n=193, 47% female) and African ancestry (AA; n=101, 59% female). RESULTS: Baseline clinical, metabolic, and inflammatory biomarkers by race and gender were consistent with epidemiological literature; pre-LPS cytokines (e.g. median (IQR) IL-6, 2.7 (2) vs.2.1 (2) pg/ml, P=0.001) were higher in AA than EA. In contrast, acute cytokine responses during endotoxemia were lower in AA than EA (e.g. median (IQR) peak IL-1RA, 30 (38) vs.43 (45) ng/ml P=0.002) as was the induction of hepatic acute-phase proteins (e.g. median (IQR) peak CRP 12.9 (9) vs.17.4 (12) mg/L P=0.005). Further, baseline levels of cytokines were only weakly correlated with peak inflammatory responses (all r(s) <0.2) both in AA and in EA. There were less pronounced and less consistent differences in the response by gender, with males having a higher AUC for CRP response compared to females (median (IQR) AUC: 185 (112) vs. 155 (118), P=0.02). CONCLUSIONS: We observed lower levels of evoked inflammation in response to endotoxin in AA compared with EA, despite similar or higher baseline levels of inflammatory markers in AA. Our data also suggest that levels of inflammatory biomarkers measured in epidemiological settings might not predict the degree of acute stress-response or risk of diseases characterized by activation of innate immunity. TRIAL REGISTRATION: FDA clinicaltrials.gov registration number NCT00953667.