Keyvan Karimi Galougahi

Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

Chronic kidney disease (CKD) affects 13% of the US population.[1][1] Although a significant proportion of these patients progress to end‐stage renal disease (ESRD) requiring renal replacement therapy (RRT)[2][2] or renal transplantation, cardiovascular disease remains the most common cause of

Redox regulation of vascular remodeling.

Vascular remodeling is a dynamic process of structural and functional changes in response to biochemical and biomechanical signals in a complex in vivo milieu. While inherently adaptive, dysregulation leads to maladaptive remodeling. Reactive oxygen species participate in homeostatic cell signaling in tightly regulated- and compartmentalized cellular circuits. It is well established that perturbations in oxidation–reduction (redox) homeostasis can lead to a state of oxidative-, and more recently, reductive stress. We provide an overview of the redox signaling in the vasculature and review the role of oxidative- and reductive stress in maladaptive vascular remodeling. Particular emphasis has been placed on essential processes that determine phenotype modulation, migration and fate of the main cell types in the vessel wall. Recent advances in systems biology and the translational opportunities they may provide to specifically target the redox pathways driving pathological vascular remodeling are discussed.

Optical coherence tomography-guided percutaneous coronary intervention in pre-terminal chronic kidney disease with no radio-contrast administration

A 67-year-old man with advanced chronic kidney disease (CKD) (creatinine = 4.5 mg/dL, eGFR = 13 mL/min/1.73 m2) not requiring haemodialysis presented with progressive angina. Diagnostic angiography with ultra-low radio-contrast volume (12 mL, contrast volume/eGFR ratio <1) revealed significant stenosis in the left anterior descending (LAD) artery ( Panel A ). The lesion was haemodynamically significant (fractional flow reserve: 0.77). Post-angiography, the …

Guiding Light: Insights Into Atherectomy by Optical Coherence Tomography

Coronary calcification presents multiple technical challenges in percutaneous coronary intervention (PCI) and is associated with suboptimal procedural results and an increase in subsequent adverse clinical events [(1)][1]. Currently, there is no standardized evidence-based strategy for PCI of

Utility of near-infrared spectroscopy for detection of thin-cap neoatherosclerosis.

Aims Near-infrared spectroscopy (NIRS) has been employed to assess the composition of the atherosclerotic plaques in native coronary arteries. However, little is known about the detection of neoatherosclerosis by NIRS in in-stent restenosis (ISR). The aim of the study was to assess the relationship between the distribution of lipid determined by NIRS and morphology of ISR on optical coherence tomography (OCT). Methods and results We performed both NIRS and OCT in 39 drug-eluting stents with ISR. Values of lipid-core burden index (LCBI) derived by NIRS were compared with the OCT-derived thickness of the fibrous cap covering neoatherosclerotic lesions. A total of 22 (49%) in-stent neointimas were identified as lipid rich by both NIRS and OCT. There was good agreement between OCT and NIRS in identifying lipid within in-stent neointima (kappa = 0.60, 95% CI: 0.34–0.86). OCT identified thin-cap neoatheromas (TCNA) (<65 µm) in 12 stents (23%). The minimal cap thickness of in-stent neoatherosclerotic plaque measured by OCT correlated with the maxLCBI4mm (maximal LCBI per 4 mm) within the stent (r = −0.77, P< 0.01). Moreover, maxLCBI4mm was able to accurately predict TCNA with a cut-off value of >144. Conclusion NIRS correlates with OCT identification of lipids in stented vessels and is able to predict the presence of thin fibrous cap neoatheroma.

Update on Intracoronary Optical Coherence Tomography: a Review of Current Concepts

Purpose of reviewThe advent of intracoronary optical coherence tomography (OCT) has been a significant leap forward in the ability to visualize coronary structures with unprecedented resolution. However, the clinical application of this imaging modality has lagged behind rapid technological advances. One of the main reasons for the lack of wider clinical uptake has been the paucity of appropriately designed prospective randomized studies to demonstrate the impact of OCT on outcome measures after percutaneous coronary intervention (PCI).Recent findingsOver the last couple of years, studies from large registries have shown the impact of OCT in decision-making in PCI, with several further reports providing valuable insights into the natural history of the atherosclerotic disease process and the modulating effects of therapies. Furthermore, guidance of PCI by OCT, including the appropriate use of newer generations of coronary stents, has been the focus of multiple studies.SummaryIn this contemporary review, we provide a brief overview of the recently published data and highlight the multiple areas that need further clarification as OCT is further incorporated into routine clinical practice.

Zero-contrast percutaneous coronary intervention on calcified lesions facilitated by rotational atherectomy: Atherectomy-assisted Zero Contrast PCI

Percutaneous coronary intervention (PCI) in patients with advanced chronic kidney disease (CKD) is challenging due to frequent presence of complex calcified lesions and the very high risk of contrast‐induced nephropathy (CIN). We report a strategy of “zero contrast” PCI, guided by intravascular imaging and physiology, performed in three patients with advanced CKD in whom severe calcification necessitated rotational atherectomy (RA) to facilitate and optimize PCI. This approach resulted in safe and successful PCI while preserving renal function.

Shedding blood: anemia and adverse events after percutaneous coronary intervention (PCI).

Substantial evidence from epidemiological studies suggests strong association between baseline anemia and worse outcomes following percutaneous coronary intervention (PCI) for both stable coronary artery disease (CAD) and acute coronary syndromes (ACS) (1-3). The existing data, almost exclusively from prospective analysis of clinical cohorts or retrospective post-hoc analysis of data from large randomized clinical trials designed to investigate other specific endpoints, point to anemia as a strong independent predictor of major adverse cardiac outcomes (MACE), major bleeding and mortality in patients undergoing PCI (4-6). Some of the published studies have utilized rigorous statistical methods to adjust for all known and measurable variables that can interact with anemia, nevertheless the associations inferred from these studies, while providing valuable insights, remain hypothesis generating.