Number of Yellow Plaques Detected in a Coronary Artery Is Associated With Future Risk of Acute Coronary Syndrome Detection of Vulnerable Patients by Angioscopy

ObjectivesWe sought to test whether the risk of acute coronary syndrome (ACS) can be estimated by angioscopy.BackgroundDisruption of vulnerable plaque and subsequent thrombosis is regarded as a major mechanism of ACS. Although yellow plaques are supposedly vulnerable, the association between angioscopically determined extent of coronary atherosclerosis and risk of ACS events has not been reported.MethodsPatients (n = 552) who received catheterization and angioscopic examination for the diagnosis of coronary artery diseases were prospectively included and followed up for new onset of ACS events. Yellow color intensities of all detected yellow plaques were graded as 1, 2, or 3 according to the standard colors. Number of yellow plaques (NYP) in a coronary artery and maximum color grade of detected yellow plaques (maxYP) were determined. Association between the incidence of ACS events and angioscopic findings were analyzed.ResultsFollow-up interval was 57.3 ± 22.1 months. Acute coronary syndrome events were detected in 39 patients (7.1%). Although maxYP was not statistically different (2.0 ± 0.7 vs. 1.8 ± 0.9; p = 0.18), NYP was higher in the patients with an ACS event than those without the event (3.1 ± 1.8 vs. 2.2 ± 1.5; p = 0.008). Patients with NYP ≥2 and those with NYP ≥5 had 2.2- and 3.8-fold higher event rates, respectively, than those with NYP 0 or 1 (9.0% and 15.6%, respectively, vs. 4.1%; p = 0.02). Multivariate logistic regression analysis revealed NYP and multivessel disease as the independent risk factors of ACS events.ConclusionsPatients with multiple yellow plaques per vessel have a higher risk of suffering ACS events than those with NYP 0 or 1. Angioscopy would be useful to detect vulnerable patients

The usefulness of nifekalant for activation mapping of premature beat-triggered atrial fibrillation: Suppression of atrial fibrillation initiation without inhibiting premature beat

AbstractA 66-year-old man underwent a second ablation for atrial fibrillation (AF). Intravenous isoproterenol administration caused the atrial premature beat (APB), triggering AF. The APB originated in the right atrium and invariably initiated AF. Therefore, contact activation mapping could not be performed without frequent electrocardioversion. To prevent the initiation of AF without inhibiting the APB firing, we administered nifekalant intravenously, which facilitated precise activation mapping and ablation of the AF-triggering APB. The administration of nifekalant may improve clinical outcomes of catheter ablation for AF triggered by non-pulmonary vein APB, which invariably initiates AF

The intestinal microbiota and cardiovascular disease

The intestinal microbiota of human hosts is the community of microorganisms living in the small and, mainly, the large intestine of humans. This microbial ecosystem has co-evolved with humans across the millennia, has come to play an important interactive role in human physiology and has been aptly called our forgotten organ. Significant properties of the microbiota benefiting its host include energy harvest from food sources indigestible by humans, protection from pathogen colonization, and vitamin synthesis. Mounting evidence has linked changes in the composition or metabolic profiles of the microbiota with human disease, including disorders of the cardiovascular spectrum. Although cause and effect mechanisms are as yet essentially unproven in the relevant literature, the established associations point to the importance of the microbiota in the pathophysiology of cardiovascular disease (CVD). In this review, we first summarize key information on the gut microbial communities and the elaborate tools developed to analyse their structure and metabolic functions. Ecological terms are explained and analytical techniques are simplified, to enhance the understanding of published studies. Statistical methods used in microbial analysis are also described in simple terms. We then present published literature on the association of the compositional and functional changes of the microbiota with CVD, including heart failure, hypertension, and atherosclerosis. Each section of the review deals with the underlying pathophysiology of the relevant associations, connecting the observational and mechanistic aspects. Finally, we discuss the challenges that remain to be met before this field of research can generate knowledge which can impact everyday clinical practice