Noninvasive detection of coronary vasospastic angina using a double-acquisition coronary CT angiography protocol in the presence and absence of an intravenous nitrate: a pilot study.

OBJECTIVES: To evaluate the feasibility of a double-acquisition coronary CT angiography (CCTA) protocol in the presence and absence of an intravenous (IV) vasodilator infusion for detecting vasospastic angina. METHODS: Twenty patients with a high clinical probability of vasospastic angina were enrolled. All subjects underwent baseline CCTA without a vasodilator in the early morning followed by a catheterized coronary angiography with ergonovine provocation test. Within 3 days, all subjects underwent repeat CCTA during a continuous IV infusion of nitrate. Vasospastic angina as detected by CCTA was defined as significant stenosis (≥50 %) with negative remodelling without definite plaques or diffuse small diameter (<2 mm) of a major coronary artery with a beaded appearance on baseline CT that completely dilated on IV nitrate CT. The CCTA results were compared to the catheterized ergonovine provocation test as the reference standard. RESULTS: Among 20 patients, the catheterized ergonovine provocation test detected vasospasm in 15 patients. The sensitivity, specificity, positive predictive value and negative predictive value of CCTA in a per-patient-based analysis were 73, 100, 100 and 56 %, respectively. CONCLUSIONS: Double-acquisition CCTA in the presence and absence of IV infusion of nitrate allows noninvasive detection of vasospastic angina with moderate sensitivity and high specificity. KEY POINTS: • Limited data exist regarding the efficacy of CCTA in detecting vasospastic angina. • We propose a double-acquisition CCTA protocol with and without IV nitrate injections. • This protocol provides 100% specificity and moderate sensitivity (73%) in spasm detection.

Gender differences in plaque characteristics of culprit lesions in patients with ST elevation myocardial infarction.

There is limited research on plaque characteristics of ST elevation myocardial infarction (STEMI) patients according to the gender and age. 280 Consecutive STEMI patients who underwent VH-IVUS imaging on culprit before percutaneous coronary intervention (PCI) were enrolled in this study. Women were significantly older than men (69.8 ± 10 vs. 55.9 ± 11.3, p < 0.001). After propensity matching, men had higher plaque burden (79.7 ± 7.8 vs. 73.7 ± 13.0 %, p = 0.010), more fibro-fatty tissue (12.8 ± 9.9 vs. 9.5 ± 6.8 %, p = 0.04) and less dense calcium than women (8.4 ± 5.8 vs. 12.3 ± 8.7 %, p = 0.007). Subgroups dividing by 50, 65, 75 years old, plaque burden was higher in elderly men aged 66-75 years compared to the young men aged less than 50 (75.5 ± 9.2 vs. 68.4 ± 10.1 %, p = 0.012). And middle aged men ranged 51-65 years showed significantly more plaque burden at minimal lumen area site than matched aged women (77.5 ± 8.0 vs. 69.0 ± 17.6 %, p = 0.012). Elderly women aged 66-75 years showed significantly more necrotic core (28.6 ± 7.3 %) and dense calcium (14.9 ± 7.5 %) compared to all the younger or matched subgroups of men. These differences in plaque composition are blunted in the very elderly of men and women aged over 75 years. The findings may explain the gender differences in clinical prognosis in STEMI patients.

Multi-modality imaging for stent edge assessment.

Optical coherence tomography (OCT) has a sufficiently high resolution to allow assessment of stent edge dissection (ED). The aims of the present study were as follows: (1) evaluation of the frequency of stent ED using OCT; (2) comparison of stent ED detection rates obtained using angiography, intravascular ultrasound (IVUS), and OCT; and (3) IVUS-Virtual Histology (IVUS-VH) evaluation of plaque composition at the site of stent EDs detected by OCT after percutaneous coronary intervention (PCI). Fifty-eight consecutive patients (59 lesions, 100 stent edges) who underwent balloon-expandable stent implantation and post-stent assessment with OCT and IVUS-VH were included. OCT revealed stent ED in 24.0 % (24 of 100) of stent edges after PCI with a balloon-expandable stent. In contrast, ED was detected in only 3.0 % (3 of 100) of stent edges using angiography and 4.0 % (4 of 100) of stent edges using IVUS. Plaque evaluation using IVUS-VH showed that the percent necrotic core (21.2 ± 8.3 vs. 13.4 ± 10.7 %, p = 0.001) and absolute dense calcium (2.9 ± 2.4 vs. 1.3 ± 2.2 mm(3), p = 0.0104) and dense calcium (13.8 ± 9.3 vs. 5.4 ± 5.8 %, p < 0.001) volumes were greater in the ED group than in the non-ED group. Thus, OCT is superior to conventional coronary angiography and IVUS in the identification of stent ED. In addition, the plaque composition at the ED site is characterized by a necrotic core and greater dense calcium levels than those observed at the non-ED site.

Better inflation time of stent balloon for second-generation drug-eluting stent expansion and apposition: an optical coherence tomography study.

OBJECTIVES: We tried to determine the effect of stent balloon inflation time on stent expansion and apposition using optical coherence tomography. BACKGROUND: Second-generation drug-eluting stents (DES) have thin struts; however, inflation times for optimal stent expansion and apposition are unknown in vivo. METHODS: Subjects included 17 patients (18 de novo coronary artery lesions), in whom Resolute Integrity → (n = 9) and Xience Prime → (n = 9) DES were deployed. All stents were inflated 3 times to the nominal inflation pressure (8.9 ± 0.6 atm) using the stent delivery balloon. The first inflation continued until the stent was angiographically fully expanded; the other 2 lasted 15 and 30 seconds, respectively. RESULTS: After the first, second, and third inflation of stent balloon, stent area (5.94 ± 1.7, 6.69 ± 1.8, 7.05 ± 1.8 mm(2) , P < 0.001) and stent volume (146.94 ± 59.40, 166.78 ± 69.55, 177.25 ± 69.19 mm(3) , P < 0.001) increased significantly. The number of malapposed struts (18.0 ± 17.0, 7.9 ± 10.2, 7.4 ± 10.8, P < 0.001) and the mean depth of malapposed struts (188.9 ± 75.6, 120.3 ± 101.4, 95.4 ± 86.8 µm, P < 0.001) decreased. Malapposed stent area (0.62 ± 0.32, 0.52 ± 0.21 mm(2) , P < 0.05) and the malapposed stent volume (15.03 ± 7.78, 12.64 ± 5.16 mm(3) , P < 0.05) decreased significantly following the second inflation; the third inflation gave no additional benefits to these parameters. There was no adverse clinical outcome after each stent balloon inflation. CONCLUSIONS: Additional 15 seconds of inflation after the angiographically full expansion of the stent balloon allows better stent expansion and apposition even though the inflation pressure is nominal pressure.

Concomitant nitrates enhance clopidogrel response during dual anti-platelet therapy.

BACKGROUND: Despite advances in modern anti-platelet strategies, clopidogrel still remains the cornerstone of dual anti-platelet therapy (DAPT) in patients undergoing percutaneous coronary interventions (PCI). There is some inconclusive evidence that response after clopidogrel may be impacted by concomitant medications, potentially affecting clinical outcomes. Sustained released nitrates (SRN) are commonly used together with clopidogrel in post-PCI setting for mild vasodilatation and nitric oxide-induced platelet inhibition. METHODS: We prospectively enrolled 458 patients (64.5 ± 9.6 years old, and 73.4% males) following PCI undergoing DAPT with clopidogrel and aspirin. Platelet reactivity was assessed by the VerifyNow™ P2Y12 assay at the maintenance outpatient setting. RESULTS: Concomitant SRN (n=266) significantly (p=0.008) enhanced platelet inhibition after DAPT (251.6 ± 80.9PRU) when compared (232.1 ± 73.5PRU) to the SRN-free (n=192) patients. Multivariate logistic regression analysis with the cut-off value of 253 PRU for defining heightened platelet reactivity confirmed independent correlation of more potent platelet inhibition during DAPT and use of SRN (Relative risk=1.675; Odds ratio [1.059-2.648]; p=0.027). In contrast, statins, calcium-channel blockers, beta blockers, angiotensin receptor blockers, ACE-inhibitors, diuretics, and anti-diabetic agents did not significantly impact platelet inhibition following DAPT. CONCLUSION: The synergic ability of SRN to enhance response during DAPT may have important clinical implications with regard to better cardiovascular protection, but extra bleeding risks, requiring further confirmation in a large randomized study.

Thienopyridine reloading in clopidogrel-loaded patients undergoing percutaneous coronary interventions: The PRAISE study.

OBJECTIVE: The impact of thienopyridine reloading on clinical outcomes, and residual high platelet reactivity (HPR) is unclear. We sought to compare the HRP-related effect of prasugrel and clopidogrel reloading in the already clopidogrel-loaded patients undergoing percutaneous coronary intervention (PCI). MATERIALS AND METHODS: In this prospective, two-center, randomized, open-label study, patients with HPR who had undergone PCI after a clopidogrel (300-600mg) loading dose (LD) were enrolled. Among screened (n=153), HPR was determined in seventy-six patients, who were randomized to either repeated clopidogrel (300mg LD, followed by 75mg MD daily) or prasugrel (20mg LD, followed by 5mg MD daily). The primary endpoint was HPR at 24h after PCI, as determined by the VerifyNow assay. The rates of sustained high and low platelet reactivity, periprocedural myocardial injury (PMI) and 30-day clinical outcomes were also assessed. RESULTS: Higher inhibition of platelet reactive units (PRU) was observed in the prasugrel group than after clopidogrel reloading (Pre-PCI: 284.4±32.0 vs 279.5±32.5, p=0.504; Post-PCI: 100.0±67.0 vs 202.9±65.8, p<0.001; 30days: 170.8±69.8 vs 215.1±62.4, p=0.007). There were less HRP post-PCI after prasugrel compared with the clopidogrel group (2.7 vs 36.1%, p<0.001). However, reloading with prasugrel did not reduce PMI compared to clopidogrel (36.8% vs 39.5%, p=0.813). CONCLUSION: Prasugrel reloading led to a greater reduction in HPR, but similar with clopidogrel PMI in post-PCI patients. Larger randomized evidence is needed for optimization of loading strategies with thienopyridines. CLINICAL TRIAL REGISTRATION INFORMATION: NCT01609647.