Unusual Presentation of Spontaneous Coronary Artery Dissection in an Older Male.

Spontaneous coronary artery dissection (SCAD) is a variant of acute coronary syndrome (ACS) that is poorly understood. SCAD has been linked to fibromuscular dysplasia (FMD), connective tissue disease (CTD), pregnancy and hormonal imbalance, systemic inflammatory conditions (e.g. IBD, vasculitis), and coronary artery vasospasm rather than traditional cardiac risk factors. Symptomology generally accompanying SCAD is indistinguishable from ACS making the timely recognition and diagnosis vital for prompt treatment. Management of SCAD is not well defined given the absence of guidelines; conservative therapy with or without invasive intervention is assessed on a case-by-case basis. In this article, we report the case of a 62-year-old male, who presented with chest pain and dyspnea on exertion and was found to have an elevated troponin-I level and corresponding electrocardiogram (EKG) findings, subsequently diagnosed with a non-ST elevation myocardial infarction (NSTEMI). Coronary angiography revealed a distal right coronary artery (RCA) dissection, which was confirmed later with intravascular ultrasound (IVUS). The patient then underwent percutaneous coronary intervention (PCI) followed by stenting of the distal RCA and was discharged on optimal medical therapy. Herein, we report a case of SCAD in an otherwise healthy male with chest pain at rest and with mild exertion without conventional cardiac risk factors.

Disparity between angiographic coronary lesion complexity and lipid core plaques assessed by near-infrared spectroscopy.

OBJECTIVE: The purpose of this study was to determine if there was a relationship between angiographic lesion complexity and the extent of lipid core plaque (LCP) identified by catheter-based near-infrared spectroscopy (NIRS). BACKGROUND: The angiographic complexity of coronary artery disease (CAD) is used to predict outcomes in patients undergoing percutaneous coronary intervention (PCI). The SYNTAX score, an angiographic tool quantifying the complexity of CAD, is associated with PCI outcomes. Recently, a novel catheter-based imaging technique using NIRS can identify LCP, which also is associated with PCI periprocedural myocardial infarction (MI). However, it is unknown whether these events are related to distinct adverse event prone pathobiology, such as a LCP within a complex angiographic lesion. Thus, we hypothesized that LCP identified by NIRS would be associated with high SYNTAX score. METHODS: Seventy-eight patients who underwent coronary angiography and target-vessel NIRS were selected from the Chemometric Observations of Lipid Core Containing Plaques of Interest in Native Coronary Arteries Registry, an industry sponsored registry to collate clinical findings in all patients undergoing NIRS evaluation. A lipid core burden index (LCBI) was obtained from the scan of the proximal 50 mm of the target vessel. Three vessel SYNTAX (total, tSYN) and target single vessel (only NIRS-interrogated vessel) SYNTAX (1vSYN) scores were calculated and compared to LCBI. High LCBI was defined as (>110) and was compared to tertile scores for 1vSYN score (low 0-5, intermediate 6-10, high ≥11) and previously established tertiles for tSYN score (low 0-22, intermediate 23-32, high ≥33). RESULTS: Patients had mean age of 63 years with prevalence of females (10%), diabetes mellitus (28%), hypertension (88%), and smoking history (72%); 1vSYN and tSYN scores correlated poorly with LCBI [(r(2) = 0.25; P = 0.02; n = 78) and (r(2) = 0.24; P = 0.04; n = 78), respectively]. Mean LCBI did not differ significantly across all tertiles of 1vSYN or tSYN scores. CONCLUSIONS: Angiographic SYNTAX score only weakly correlated with LCBI. It is of interest as well that high LCBI was also present in cases of low SYNTAX scores. The disparity between the degree of angiographic complexity and the amount of LCP supports postulated mechanisms of the adverse event propensity even in patients who demonstrate low angiographic complexity. Future studies are necessary to address the clinical significance of high LCBI in patients with low-to-intermediate angiographic complexity and their potential for PCI-related complications.

Molecular imaging of human ACE-1 expression in transgenic rats.

OBJECTIVES: The aim of this study was to develop a molecular imaging strategy that can monitor myocardial angiotensin-converting enzyme (ACE)-1 upregulation as a function of progressive heart failure. BACKGROUND: High-affinity technetium-99m-labeled lisinopril (Tc-Lis) has been shown to specifically localize in tissues that express ACE in vivo, such as the lungs. Whether Tc-Lis can also detect upregulation of ACE in the heart, by external in vivo imaging, has not been established. METHODS: Twenty-one ACE-1 over-expressing transgenic (Tg) and 18 wild-type control rats were imaged using in vivo micro single-positron emission computed tomography (SPECT)-computed tomography (CT) at 10, 30, 60, and 120 min after Tc-Lis injection. A subgroup of rats received nonradiolabeled (cold) lisinopril before the Tc-Lis injection to evaluate nonspecific binding. After imaging, the rat myocardium was explanted, ex vivo images were acquired, and percent injected dose per gram gamma-well was counted, followed by an assessment of enzyme-linked immunosorbent assay-verified ACE activity and messenger ribonucleic acid expression. RESULTS: On micro SPECT-CT, myocardial ACE-1 uptake was best visualized in Tg rats at 120 min after Tc-Lis injection. The quantitative uptake of Tc-Lis in the myocardium was 5-fold higher in mutant Tg than in control rats at each time point after tracer injection. The percent injected dose per gram uptake was 0.74 ± 0.13 in Tg myocardium at 30 min and was reduced substantially to 0.034 ± 0.003% when pre-treated with cold lisinopril (p = 0.029). Enzyme activity assay showed a >30-fold higher level of ACE-1 activity in the myocardium of Tg rats than in controls. The ACE-1 messenger ribonucleic acid was quantified, and lisinopril was found to have no effect on ACE-1 gene expression. CONCLUSIONS: The Tc-Lis binds specifically to ACE, and the activity can be localized in Tg rat hearts that over-express human ACE-1 with a signal intensity that is sufficiently high to allow external imaging. Such a molecular imaging strategy may help identify susceptibility to heart failure and may allow optimization of pharmacologic intervention.