Gulati, Rajiv

Embolic protection devices are occasionally employed during endovascular interventions to prevent complications caused by embolic debris. However, these devices have imperfect efficacy, confer risk of endovascular trauma, and are expensive. We report a patient with giant cell arteritis and symptomatic axillary artery stenosis, with a perceived elevated risk of distal embolization during endovascular intervention. We describe a straightforward embolic protection technique of brachial pressure cuff inflation during endovascular intervention and aspiration of displaced thrombotic material from the static column of blood. This novel, effective, and cost-free technique could also be employed in other vascular beds during endovascular intervention.

Ultrasound (US) enhancement of plasmid-based gene transfer is an emerging technique. Our hypothesis was that two contrast agents (Optison and PESDA), and two US exposure modalities (dedicated continuous wave system and diagnostic scanner) may have different effects. Luciferase plasmid with or without contrast agent was added to vascular smooth muscle cells and endothelial cells, followed by US exposure. Luciferase activity was measured 24 h later. US exposure consistently induced higher transfection rates than all controls. PESDA was superior to Optison in both cell lines. In vitro, continuous wave and diagnostic US were not significantly different. In vivo, Lux and PESDA were injected into skeletal muscles of rats (IM or intra-arterial) followed or not by US exposure. In separate animals, adenovirus encoding for luciferase was injected IM and was not followed by US exposure. Gene transfer efficacy was 8–10 fold higher with US and PESDA than with plasmid alone, but 2 fold lower than with adenovirus. However, as opposed to adenovirus, US-enhanced plasmid gene transfer was highly localized to the injected muscle, with no expression at distal sites. Our results support the hypothesis that contrast agents and exposure modalities are not equivalent with regard to gene transfer efficacy.

Background— High sensitivity C-reactive protein (hsCRP) has been identified as a predictor of adverse cardiovascular outcomes. Whether hsCRP is a useful biomarker for risk stratification in contemporary percutaneous coronary intervention remains unknown. Methods and Results— We conducted a prospective study among 513 patients undergoing non-emergency percutaneous coronary intervention and examined the relationship between pre- and postprocedural hsCRP levels and outcomes. The patients were divided according to the median preprocedural hsCRP level (0.3 mg/dL). Patients with high hsCRP had significantly more adverse clinical characteristics. Preprocedural hsCRP level was an independent predictor of periprocedural myocardial infarction (odds ratio per doubling of hsCRP 1.15 [95% confidence interval, 1.01–1.31]; P =0.038). Unadjusted mortality (29.7% versus 9.9%; P <0.001) and the combined end point of death or myocardial infarction (36.5% versus 16.0%, P <0.001) during a follow-up of 5 years were markedly greater in patients with high preprocedural hsCRP. Similar relationships existed for postprocedural hsCRP. However, after multivariable adjustment, neither preprocedural hsCRP levels (hazard ratio per doubling 0.96 [0.92, 1.00]; P =0.066) nor postprocedural hsCRP levels (hazard ratio 0.98 [0.94, 1.02]; P =0.27) were significantly associated with mortality. Conclusions— High hsCRP is associated with a greater independent risk of periprocedural myocardial infarction, as defined by the universal definition, but is not an independent determinant of mortality after percutaneous coronary intervention. Our findings suggest that routine measurement of hsCRP in patients undergoing percutaneous coronary intervention in contemporary practice is unlikely to be beneficial.

Background— Coronary stents, drug-eluting stents in particular, have been linked to coronary epicardial endothelial dysfunction after implantation. However, less is known about their impact on coronary microvascular function and their long-term effects on the vasculature. Methods and Results— We evaluated 71 patients (mean age, 53.0±10.1 years) with chest pain and angiographically nonsignificant coronary artery disease 17.1±17.1 months after left anterior descending coronary artery stenting. Seventy-one age- and sex-matched patients (mean age, 53.0±10.3 years) with chest pain but no prior coronary intervention served as controls. Coronary blood flow in response to the endothelium-dependent vasodilator acetylcholine as well as the microvascular (endothelium-independent) coronary flow reserve in response to intracoronary adenosine were evaluated. Quantitative coronary angiography was used to study epicardial diameter changes to acetylcholine. Microcirculatory function was not significantly different between the stenting and control groups (median [interquartile range] coronary flow reserve, 2.9 [2.5–3.4] versus 3.0 [2.4–3.4] mL/min, P =0.24; change of coronary blood flow, 34.9% [−34.4% to 90.0%] versus 54.7% [−5.6% to 104.6%], P =0.18). Both groups exhibited epicardial endothelial dysfunction (−23.0% [−47.4% to −7.6%] versus −20.0% [−40.0% to 0.0%], P =0.4). Results did not differ between patients with drug-eluting stents (n=46) and patients with bare-metal stents (n=24). Conclusions— This study demonstrates that in patients with coronary arteries in which a stent has been placed, coronary microcirculatory and epicardial vascular function are not significantly different from that of an age- and sex-matched population with similar symptoms but nonsignificant coronary artery disease.

Background— Spontaneous coronary artery dissection (SCAD) is an acute coronary event of uncertain origin. Clinical features and prognosis remain insufficiently characterized. Methods and Results— A retrospective single-center cohort study identified 87 patients with angiographically confirmed SCAD. Incidence, clinical characteristics, treatment modalities, in-hospital outcomes, and long-term risk of SCAD recurrence or major adverse cardiac events were evaluated. Mean age was 42.6 years; 82% were female. Extreme exertion at SCAD onset was more frequent in men (7 of 16 versus 2 of 71; P <0.001), and postpartum status was observed in 13 of 71 women (18%). Presentation was ST-elevation myocardial infarction in 49%. Multivessel SCAD was found in 23%. Initial conservative management (31 of 87) and coronary artery bypass grafting (7 of 87) were associated with an uncomplicated in-hospital course, whereas percutaneous coronary intervention was complicated by technical failure in 15 of 43 patients (35%) and 1 death. During a median follow-up of 47 months (interquartile range, 18–106 months), SCAD recurred in 15 patients, all female. Estimated 10-year rate of major adverse cardiac events (death, heart failure, myocardial infarction, and SCAD recurrence) was 47%. Fibromuscular dysplasia of the iliac artery was identified incidentally in 8 of 16 femoral angiograms (50%) undertaken before closure device placement and in the carotid arteries of 2 others with carotid dissection. Conclusions— SCAD affects a young, predominantly female population, frequently presenting as ST-elevation myocardial infarction. Although in-hospital mortality is low regardless of initial treatment, percutaneous coronary intervention is associated with high rates of complication. Risks of SCAD recurrence and major adverse cardiac events in the long term emphasize the need for close follow-up. Fibromuscular dysplasia is a novel association and potentially causative factor.

Background— Clinical outcomes after stent placement in patients with a history of metal allergy remain incompletely understood. We performed a single-center retrospective study to evaluate such outcomes. Methods and Results— Twenty-nine allergic patients who underwent coronary stent implantation were compared with a nonallergic group (n=250) matched for demographics and a propensity score for allergy to metal. Hypersensitivity to nickel was reported in 26 of 29 and chromium in 9 of 29. Patch testing performed in 11 of 29 patients was positive in all. Comparing allergy versus control subjects, there were no differences in number of segments treated (1.4±0.7 versus 1.5±0.7), stents placed (1.7±1.1 versus 1.6±0.9), and frequency of drug-eluting stent usage (52% versus 60%). In-hospital death (0% versus 0%), myocardial infarction (MI, 4% versus 3%, P =0.27), and 30-day death (3% versus 0%, P =0.53) and MI (3% versus 4%, P =0.71) were statistically similar. There were no differences in 4-year death (12% versus 13%), target lesion revascularization (TLR, 13 versus 17%, P =0.54), or death/MI/TLR (24% versus 34%, P =0.20). Clinically driven repeat angiography in 12 of 29 allergy patients revealed binary restenosis rates of 27% in bare metal stents and 0% in drug-eluting stents, with mean diameter in-stent restenosis of 36% and 8%, respectively. There was no change in circulating eosinophil and lymphocyte counts after stenting in the allergy group (0.19–0.20, P =0.67, and 1.90–1.79, P =0.59, respectively). Conclusions— A history of metal allergy was not associated with adverse early or late outcomes in this single-center study.