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Despite the intense efforts to prevent programmers from writing code with memory errors, memory corruption vulnerabilities are still a major security threat. Consequently, control-flow integrity has received significant attention in the research community, and software developers to combat control code execution attacks in the presence of type of faults. Control-flow Integrity (CFI) is a large family of techniques that aims to eradicate memory error exploitation by ensuring that the instruction pointer (IP) of a running process cannot be controlled by a malicious attacker. In this paper, we assess the effectiveness of 14 CFI techniques against the most popular exploitation techniques, including code reuse attacks, return-to-user, return-to-libc, and replay attacks. We also classify these techniques based on their security, robustness, and implementation complexity. Our study indicates that the majority of the CFI techniques are primarily focused on restricting indirect branch instructions and cannot prevent all forms of vulnerability exploitation. We conclude that the performance overhead introduced, jointly with the partial attack coverage, is discouraging the industry from adopting most of them.

Objectives: To determine the influence of diabetes mellitus on coronary collateral flow by accurate means of collateral flow measurement in a large population with variable degrees of coronary artery disease. Methods: 200 patients (mean (SD) age 64 (9) years; 100 diabetic and 100 non-diabetic) were enrolled in the study. Coronary collateral flow was assessed in 174 stenotic and in 26 angiographically normal vessels with a pressure guidewire (n  =  131), Doppler guidewire (n  =  36), or both (n  =  33) to calculate pressure or flow velocity derived collateral flow index (CFI). Diabetic patients were perfectly matched with a non-diabetic control group for clinical, haemodynamic, and angiographic parameters. Results: CFI did not differ between the diabetic and the non-diabetic patients (0.21 (0.12) v 0.19 (0.13), not significant). Likewise, CFI did not differ when only angiographically normal vessels (0.20 (0.09) v 0.15 (0.08), not significant) or chronic total coronary occlusions (0.30 (0.14) v 0.30 (0.17), not significant) were compared. Fewer patients in the diabetic group tended to have angina pectoris during the one minute vessel occlusion (60 diabetic v 69 non-diabetic patients, p  =  0.15). Conclusion: Quantitatively measured coronary CFI did not differ between diabetic and non-diabetic patients with stable coronary artery disease.

Objective: To evaluate whether a well developed collateral circulation predisposes to restenosis after percutaneous coronary intervention (PCI). Design: Prospective observational study. Patients and setting: 58 patients undergoing elective single vessel PCI in a tertiary referral interventional cardiac unit in the UK. Methods: Collateral flow index (CFI) was calculated as (Pw − Pv)/(Pa − Pv), where Pa, Pw, and Pv are aortic, coronary wedge, and right atrial pressures during maximum hyperaemia. Collateral supply was considered poor (CFI < 0.25) or good (CFI ⩾ 0.25). Main outcome measures: In-stent restenosis six months after PCI, classified as neointimal volume ⩾ 25% stent volume on intravascular ultrasound (IVUS), or minimum lumen area ⩽ 50% stent area on IVUS, or minimum lumen diameter ⩽ 50% reference vessel diameter on quantitative coronary angiography. Results: Patients with good collaterals had more severe coronary stenoses at baseline (90 (11)% v 75 (16)%, p < 0.001). Restenosis rates were similar in poor and good collateral groups (35% v 43%, p  =  0.76 for diameter restenosis, 27% v 45%, p  =  0.34 for area restenosis, and 23% v 24%, p  =  0.84 for volumetric restenosis). CFI was not correlated with diameter, area, or volumetric restenosis (r2 < 0.1 for each). By multivariate analysis, stent diameter, stent length, > 10% residual stenosis, and smoking history were predictive of restenosis. Conclusion: A well developed collateral circulation does not predict an increased risk of restenosis after PCI.

[...]remodelling of pre-existing collateral vessels (arteriogenesis) proves possible even in the face of normal coronary circulation.

[...]this large clinical study in 500 patients with coronary artery disease reveals no effect of statins on coronary collateral flow.

Objective: To determine whether the changes in the manifestations of myocardial ischaemia during sequential angina episodes caused by exercise or coronary artery occlusion are collateral dependent. Methods: 40 patients awaiting percutaneous transluminal coronary angioplasty for an isolated left anterior descending artery stenosis underwent three sequential treadmill exercise tests, with the second exertion separated from the first by 15 minutes, and from the third by 90 minutes; 28 patients subsequently completed two (> 180 s) sequential intracoronary balloon inflations with measurement of collateral flow index from mean coronary artery wedge, aortic, and coronary sinus pressures. Results: On second compared with first exercise, time to 0.1 mV ST depression (mean (SD): 340 (27) v 266 (25) s) and rate–pressure product at 0.1 mV ST depression (22 068 (725) v 19 586 (584) beats/min/mm Hg) were increased (all p < 0.005), while angina and ventricular ectopic beat frequency were diminished (p < 0.05). This advantage, which had waned by the third effort, was independent of collateral flow index. Similarly, at the end of the second compared with the first coronary occlusion, ventricular tachycardia (21% v 0%, p < 0.05), ST elevation (0.47 (0.07) v 0.33 (0.05) mV, p < 0.005), and angina severity (6.1 (0.7) v 4.6 (0.7) units, p < 0.005) were reduced despite similar collateral flow indices. Conclusions: In patients with coronary artery disease, ventricular arrhythmias, ST deviation, and angina are reduced during a second exertion or during a second coronary occlusion. This protective effect can occur independently of collateral recruitment. These characteristics, together with the breadth and temporal pattern of protection, are consistent with ischaemic preconditioning.

Objective: To test the hypothesis that regional left ventricular (LV) function during balloon angioplasty is related to the amount of collateral flow to the ischaemic region. Design: Prospective study. Setting: Tertiary referral centre. Methods: In 50 patients with coronary artery disease and without myocardial infarction, regional systolic and diastolic LV function was determined using tissue Doppler ultrasound (TD) before and at the end of a 60 second occlusion of a stenotic lesion undergoing percutaneous transluminal coronary angioplasty (PTCA) through a pressure guidewire. The study population was subdivided into a group with collaterals insufficient (n = 33) and one with collaterals sufficient (n = 17) to prevent ECG ST shifts suggestive of myocardial ischaemia during PTCA. Pulsed TD was performed from an apical window in the myocardial region supplied by the vessel being treated by PTCA. Pressure derived collateral flow index (CFI) was determined by simultaneous measurement of mean aortic (Pao) and distal intracoronary occlusive pressures (Poccl), where CFI = (Poccl − 8)/(Pao − 8). Results: At 60 seconds of occlusion, several parameters of systolic and diastolic TD derived LV long axis function were significantly different between the groups. Also, there was a significant correlation between regional systolic excursion velocity, early diastolic excursion velocity, regional isovolumetric relaxation time, and CFI. Conclusion: During brief coronary artery occlusions, regional systolic and diastolic LV function is directly related to the amount of collateral flow to this territory.