Ali Pourdjabbar

Natural History and Management of Aortocoronary Saphenous Vein Graft Aneurysms A Systematic Review of Published Cases

Despite ongoing advances in percutaneous revascularization, coronary artery bypass grafting (CABG) continues to be performed in a large number of patients, with >400 000 operations reported in 2007 in the United States alone.1 Although arterial conduits are generally preferred, saphenous vein grafts (SVGs) continue to be used regularly. First described by Riahi and colleagues2 in 1975, aneurysmal dilatation of aortocoronary SVGs remains a rare yet widely reported phenomenon. Indeed, subsequent literature on the topic consists almost exclusively of case reports and small case series. Thus, the precise incidence of aortocoronary SVG aneurysms (SVGAs) remains difficult to ascertain, although in 1 case series, an incidence of 0.07% was estimated from a review of >5500 grafts at a single institution.3 However, this likely underestimates the true number because SVGAs often remain clinically silent and no guidelines exist to screen for their development. Given the infrequent identification of SVGAs, our current understanding of the epidemiology and pathogenesis of these aneurysms remains limited. Aneurysms are generally defined as a focal dilatation of vessels >1.5 times the proximal reference diameter; however, aneurysmal dilatation of aortocoronary SVGs has led to “giant” aneurysm formation, with reports of cases exceeding 10 cm.4–6 SVGAs are often incidentally identified on imaging, but cases of rupture,7 fistula formation with neighboring anatomy,8 and hemodynamic compromise resulting from compression of adjacent cardiac and vascular structures have been reported.9 To date, 2 reviews have been published that briefly summarize 108 cases of SVGAs.10,11 Traditionally, their management has been surgical—generally resection of the aneurysm with or without bypass of the affected territory. However, with refinement of percutaneous techniques, including the use of Amplatzer devices, covered stents, and arterial coiling, the management options …

Pathogenesis of Neointima Formation Following Vascular Injury

Revascularization remains the cornerstone of managing obstructive coronary artery disease. Although percutaneous coronary interventions involving the insertion of metal scaffolds, known as stents, has emerged as the preferred method of restoring vessel patency, as many as 30% of patients will experience a gradual re-narrowing of the lumen caused by neointima (NI) formation, resulting in a condition known as in-stent restenosis (ISR). ISR represents a significant limitation to percutaneous revascularization - however, abrogating NI formation following stent implantation has been hampered by an incomplete understanding of the pathogenesis of in-stent lesions. While numerous mechanisms have been proposed to explain the pathogenesis of ISR, data from human and animal models have yielded conflicting results. Herein, we review key studies of NI development following vascular injury with a focus on the origin of cells participating in NI formation.

Lack of S100A1 in mice confers a gender-dependent hypertensive phenotype and increased mortality after myocardial infarction

S100A1 is a small Ca(2+)-binding protein expressed in the myocardium and blood vessels that is downregulated in the diseased heart and plays a role in the regulation of cardiac muscle Ca(2+) homeostasis and contractility. To understand its physiological role under basal conditions and after myocardial infarction (MI), we used a mouse strain with targeted deletion of the S100A1 gene [S100A1 knockout (KO) mice]. We compared 49 wild-type (WT) and 56 S100A1 KO mice (6-8 wk old) over 28 days after MI with sham-operated controls. We also examined the effect of S100A1 deficiency on vascular function of isolated blood vessels. S100A1 KO mice demonstrated worse survival compared with WT mice (21% vs. 69%, respectively, P < 0.001). Hemodynamic evaluation revealed a higher mean arterial pressure (MAP) in sham-operated KO animals compared with WT animals (99 +/- 4 vs. 77 +/- 3 mmHg, respectively, P < 0.001) that persisted in both groups after MI (86 +/- 2 vs. 66 +/- 4 mmHg, respectively, P < 0.001). Sham-operated male S100A1 KO mice had higher MAP than female KO mice (122 +/- 5 vs. 93 +/- 3 mmHg, respectively P < 0.05) and reduced survival after MI (4% vs. 27%, respectively, P < 0.05). In isolated aortas and mesenteric arteries, ACh-evoked vasodilatation in KO mice was significantly reduced compared with WT mice (P < 0.05). Nitric oxide production was reduced in endothelial cells isolated from KO mice. Thus, absence of S100A1 results in acute functional impairment and high mortality after MI associated with a gender-specific hypertensive phenotype. S100A1 appears to play a role in the endothelium-dependent regulation of blood pressure.

Progenitor Cells for Arterial Repair: Incremental Advancements towards Therapeutic Reality

Coronary revascularization remains the standard treatment for obstructive coronary artery disease and can be accomplished by either percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery. Considerable advances have rendered PCI the most common form of revascularization and improved clinical outcomes. However, numerous challenges to modern PCI remain, namely, in-stent restenosis and stent thrombosis, underscoring the importance of understanding the vessel wall response to injury to identify targets for intervention. Among recent promising discoveries, endothelial progenitor cells (EPCs) have garnered considerable interest given an increasing appreciation of their role in vascular homeostasis and their ability to promote vascular repair after stent placement. Circulating EPC numbers have been inversely correlated with cardiovascular risk, while administration of EPCs in humans has demonstrated improved clinical outcomes. Despite these encouraging results, however, advancing EPCs as a therapeutic modality has been hampered by a fundamental roadblock: what constitutes an EPC? We review current definitions and sources of EPCs as well as the proposed mechanisms of EPC-mediated vascular repair. Additionally, we discuss the current state of EPCs as therapeutic agents, focusing on endogenous augmentation and transplantation.

Photoplethysmography using a smartphone application for assessment of ulnar artery patency: a randomized clinical trial

BACKGROUND: Radial artery access is commonly performed for coronary angiography and invasive hemodynamic monitoring. Despite limitations in diagnostic accuracy, the modified Allen test (manual occlusion of radial and ulnar arteries followed by release of the latter and assessment of palmar blush) is used routinely to evaluate the collateral circulation to the hand and, therefore, to determine patient eligibility for radial artery access. We sought to evaluate whether a smartphone application may provide a superior alternative to the modified Allen test. METHODS: We compared the modified Allen test with a smartphone heart rate–monitoring application (photoplethysmography readings detected using a smartphone camera lens placed on the patient’s index finger) in patients undergoing a planned cardiac catheterization. Test order was randomly assigned in a 1:1 fashion. All patients then underwent conventional plethysmography of the index finger, followed by Doppler ultrasonography of the radial and ulnar arteries (the diagnostic standard). The primary outcome was diagnostic accuracy of the heart rate–monitoring application. RESULTS: Among 438 patients who were included in the study, we found that the heart rate–monitoring application had a superior diagnostic accuracy compared with the modified Allen test (91.8% v. 81.7%, p = 0.002), attributable to its greater specificity (93.0% v. 82.8%, p = 0.001). We also found that this application had greater diagnostic accuracy for assessment of radial or ulnar artery patency in the ipsilateral and contralateral wrist (94.0% v. 84.0%, p < 0.001). INTERPRETATION: A smartphone application used at the bedside was diagnostically superior to traditional physical examination for confirming ulnar patency before radial artery access. This study highlights the potential for smartphone-based diagnostics to aid in clinical decision-making at the patient’s bedside. Trial registration: Clinicaltrials.gov, no. NCT02519491.