Donisan, Teodora

Introduction: Spontaneous coronary artery dissection (SCAD) is a poorly understood cause of acute coronary syndrome (ACS), predominantly affecting young women and frequently related to acute stressors. It has been suggested that stress induced cardiomyopathy can cause dissection via mechanical distortion of the vessel at wall-motion hinge points. Whether specific coronary anatomic configurations also predispose to distortion and hence SCAD remains unknown. Hypothesis: Patients with left anterior descending (LAD) SCAD have a higher frequency of a “wrap around” (type IV - perfuses >25% of the inferior wall) LAD. Methods: Coronary angiograms of patients in the Mayo Clinic SCAD Registry were reviewed. Patients from functional angiogram registry with similar characteristics were used as controls. Patients with an LAD SCAD were compared to patients who never had an LAD SCAD. For identifying predictors of LAD SCAD, patients who never had an LAD SCAD were compared to patients that had an LAD SCAD as a recurrent event, but not as the initial presentation. Results: A total of 456 patients with SCAD (46±6 years; 96% women) were included. The control group consisted of 178 patients (44±7 years, 97% women). Type IV LAD was more common in the SCAD cohort (Figure 1), and patients in the LAD SCAD group had a higher proportion of type IV LAD when compared to non-LAD SCAD (47.6% vs 23.0% p < 0.001). Bifurcation involvement was also more frequent (48.6 vs 25.8%, p <0.001). Individual predictors of an LAD SCAD during follow-up were diagnosis of hypertension, peripartum SCAD, involvement of a bifurcation and type IV LAD. After multivariate analysis, only bifurcation involvement (OR 2.49, p = 0.01) and type IV LAD (OR 2.26, p = 0.02) remained as predictors of LAD SCAD during follow-up. In patients in whom the PDA perfused the apex (LAD I and II), PDA was more likely to be involved by SCAD (OR 6.17, p<0.001). There were no other differences in coronary distribution after stratifying by LAD types. Conclusions: Type IV LAD variant is more common in patients with LAD SCAD. This finding suggests that coronary anatomic variants predispose to SCAD and lend further support to the mechanical distortion hypothesis.

Abstract Background Chimeric antigen receptor (CAR) T-cell therapy has been revolutionary in the treatment of blood cancers, but has been associated with arrhythmias such as atrial fibrillation (AF). Whether the incidence of AF has changed over time and if contributing risk factors are present remains to be defined. Methods Leveraging the Mayo Electronic Medical Record, we extracted a cohort of patients who underwent CAR T-cell therapy between 2016 and 2022. From this cohort, we identified those who had a diagnosis of AF at any point. We then defined the endpoint of interest as the first episode of new or recurrent AF during or after CAR T-cell infusion. Fine and Gray subdistribution hazard modeling was used to calculate the association of patient characteristics to the endpoint of interest. Variables with P&lt;0.20 in univariate modeling were chosen for the multivariate model. Significance was defined as P&lt;0.05. Results There were 328 patients who underwent CAR T-cell therapy between 2016 and 2022. Of this cohort, 27 (8.2%) patients had a pre-existing diagnosis of AF, of which 6 had recurrence of AF after CAR T (22.2%), while 21 (77.8%) did not. Of the 301 patients without a prior history of AF, 8 (2.7%) patients developed new-onset AF after CAR T. The majority of the 14 new or recurrent AF events (4.3% overall incidence) occurred within 30 days of receiving CAR T (N=10, 71.4%), the remainder after 180 days (Figure 1). No trend in declining incidence over time was noted. Prior AF, neurotoxicity, and inflammation (cytokine release syndrome and macrophage activating syndrome-like (MAS-L)) were strongly associated with the risk of developing new or recurrent AF (Table 1). Only presence of MAS-L remained an independent predictor in the multivariate model (HR 15.4, 95% CI 3.9-61.2, P&lt;0.001). Conclusion AF is mainly seen early following CAR T-cell therapy, and mainly in association with severe inflammatory responses. Early and aggressive treatment of CRS and MAS-L may be recommendable for patients undergoing CAR-T therapy, especially for those with a prior history of AF.

Background and Objectives: Cancer and coronary artery disease (CAD) often coexist. Compared to quantitative coronary angiography (QCA), fractional flow reserve (FFR) has emerged as a more reliable method of identifying significant coronary stenoses. We aimed to assess the specific management, safety and outcomes of FFR-guided percutaneous coronary intervention (PCI) in cancer patients with stable CAD. Materials and Methods: FFR was used to assess cancer patients that underwent coronary angiography for stable CAD between September 2008 and May 2016, and were found to have ≥50% stenosis by QCA. Patients with lesions with an FFR > 0.75 received medical therapy alone, while those with FFR ≤ 0.75 were revascularized. Procedure-related complications, all-cause mortality, nonfatal myocardial infarction, or urgent revascularizations were analyzed. Results: Fifty-seven patients with stable CAD underwent FFR on 57 lesions. Out of 31 patients with ≥70% stenosis as measured by QCA, 14 (45.1%) had an FFR ≥ 0.75 and lesions were reclassified as moderate and did not receive PCI nor DAPT. Out of 26 patients with <70% stenosis as measured by QCA, 6 (23%) had an FFR < 0.75 and were reclassified as severe and were treated with PCI and associated DAPT. No periprocedural complications, urgent revascularization, acute coronary syndromes, or cardiovascular deaths were noted. There was a 22.8% mortality at 1 year, all cancer related. Patients who received a stent by FFR assessment showed a significant association with decreased risk of all-cause death (HR: 0.37, 95% CI 0.15–0.90, p = 0.03). Conclusions: Further studies are needed to define the optimal therapeutic approach for cancer patients with CAD. Using an FFR cut-off point of 0.75 to guide PCI translates into fewer interventions and can facilitate cancer care. There was an overall reduction in mortality in patients that received a stent, suggesting increased resilience to cancer therapy and progression.

In patients with cancer, myocardial infarction (MI) has distinct features and mechanisms compared to the non-oncology population. Triggers of myocardial ischemia specific to the oncology population have been increasingly identified. Coronary plaque disruption, coronary vasospasm, coronary microvascular dysfunction, spontaneous coronary artery dissection, and coronary oxygen supply-demand mismatch are all causes of MI that have been shown to have specific triggers related to either the treatments or complications of cancer. MI can occur in the presence or absence of atherosclerotic coronary artery disease (CAD). MI with nonobstructive CAD (MINOCA) is a heterogeneous syndrome that has distinct pathophysiology and different epidemiology from MI with significant CAD (MI-CAD). Recognition and differentiation of MI-CAD and MINOCA is essential in the oncology population, due to unique etiology and impact on diagnosis, management, and overall outcomes. There are currently no reports in the literature concerning MINOCA as a unified syndrome in oncology patients. The purpose of this review is to analyze the literature for studies related to known triggers of myocardial ischemia in cancer patients, with a focus on MINOCA. We propose that certain cancer treatments can induce MINOCA-like states, and further research is warranted to investigate mechanisms that may be unique to certain cancer states and types of treatment.