Background—: Discordance between fractional flow reserve (FFR) and coronary flow velocity reserve (CFVR) may reflect important coronary pathophysiology but usually remains unnoticed in clinical practice. We evaluated the physiological basis and clinical outcome associated with FFR/CFVR discordance. Methods and Results—: We studied 157 intermediate coronary stenoses in 157 patients, evaluated by FFR and CFVR between April 1997 and September 2006 in which revascularization was deferred. Long-term follow-up was performed to document the occurrence of major adverse cardiac events: cardiac death, myocardial infarction, or target vessel revascularization. Discordance between FFR and CFVR occurred in 31% and 37% of stenoses at the 0.75, and 0.80 FFR cut-off value, respectively, and was characterized by microvascular resistances during basal and hyperemic conditions. Follow-up duration amounted to 11.7 years (Q1–Q3, 9.9–13.3 years). Compared with concordant normal results of FFR and CFVR, a normal FFR with an abnormal CFVR was associated with significantly increased major adverse cardiac events rate throughout 10 years of follow-up, regardless of the FFR cut-off applied. In contrast, an abnormal FFR with a normal CFVR was associated with equivalent clinical outcome compared with concordant normal results: ≤3 years when FFR <0.75 was depicted abnormal and throughout 10 years of follow-up when FFR ≤0.80 was depicted abnormal. Conclusions—: Discordance of CFVR with FFR originates from the involvement of the coronary microvasculature. Importantly, the risk for major adverse cardiac events associated with FFR/CFVR discordance is mainly attributable to stenoses where CFVR is abnormal. This emphasizes the requirement of intracoronary flow assessment in addition to coronary pressure for optimal risk stratification in stable coronary artery disease.

The roles of anticoagulation alone or with an antiplatelet agent after transcatheter aortic-valve implantation (TAVI) have not been well studied.

Monocytes are critical mediators of healing following acute myocardial infarction (AMI), making them an interesting target to improve myocardial repair. The purpose of this study was a gain of insight into the source and recruitment of monocytes following AMI in humans. Post-mortem tissue specimens of myocardium, spleen and bone marrow were collected from 28 patients who died at different time points after AMI. Twelve patients who died from other causes served as controls. The presence and localization of monocytes (CD14⁺ cells), and their CD14⁺CD16^– and CD14⁺CD16⁺ subsets, were evaluated by immunohistochemical and immunofluorescence analyses. CD14⁺ cells localized at distinct regions of the infarcted myocardium in different phases of healing following AMI. In the inflammatory phase after AMI, CD14⁺ cells were predominantly located in the infarct border zone, adjacent to cardiomyocytes, and consisted for 85% (78–92%) of CD14⁺CD16^– cells. In contrast, in the subsequent post-AMI proliferative phase, massive accumulation of CD14⁺ cells was observed in the infarct core, containing comparable proportions of both the CD14⁺CD16^– [60% (31–67%)] and CD14⁺CD16⁺ subsets [40% (33–69%)]. Importantly, in AMI patients, of the number of CD14⁺ cells was decreased by 39% in the bone marrow and by 58% in the spleen, in comparison with control patients (P = 0.02 and <0.001, respectively). Overall, this study showed a unique spatiotemporal pattern of monocyte accumulation in the human myocardium following AMI that coincides with a marked depletion of monocytes from the spleen, suggesting that the human spleen contains an important reservoir function for monocytes.

Cognitive impairment is common in patients with cardiovascular disease. One in 3 patients presenting at cardiology clinics have some degree of cognitive impairment, depending on the cardiac condition, comorbidities, and age. In up to half of these cases cognitive impairment may go unrecognized; however, it may affect self-management and treatment adherence. The high prevalence of cognitive impairment in patients with cardiac disease is likely due to shared risk factors, as well as direct consequences of cardiac dysfunction on the brain. Moreover, cardiac interventions may have beneficial as well as adverse effects on cognitive functioning. In this review, we describe prevalence and risk factors for cognitive impairment in patients with several common cardiac conditions: heart failure, coronary artery disease, and aortic valve stenosis. We discuss the potential effects of guideline-based treatments on cognition and identify open questions and unmet needs. Given the high prevalence of unrecognized cognitive impairment in cardiac patients, we recommend a stepwise approach to improve detection and management of cognitive impairment.