Quantitative flow ratio or angiography for the assessment of non-culprit lesions in acute coronary syndromes, a randomized trial.

BACKGROUND: Patients undergoing percutaneous coronary intervention for acute coronary syndromes often have multivessel disease (MVD). Quantitative flow ratio (QFR) is an angiography-based technology that may help quantify the functional significance of non-culprit lesions, with the advantage that measurements are possible also once the patient is discharged from the catheterization laboratory. AIM: Our two-center, randomized superiority trial aimed to test whether QFR, as compared to angiography, modifies the rate of non-culprit lesion interventions (primary functional endpoint) and improves the outcomes of patients with acute coronary syndromes and MVD (primary clinical endpoint). METHODS: In total, 202 consecutive patients (64 [56-71] years of age, 160 men) with STEMI (n = 69 (34%)), NSTEMI (n = 94 (47%)), or unstable angina (n = 39 (19%)) and MVD who had undergone successful treatment of all culprit lesions were randomized 1:1 to angiography- vs. QFR-guided delayed revascularization of 246 non-culprit stenoses (1.2/patient). RESULTS: The proportion of patients assigned to percutaneous intervention was not different between groups (angiography group: 45 (45%) vs. QFR: 56 (55%), P = 0.125; relative risk = 0.80 (0.60-1.06)). At 12 months, a primary clinical endpoint event (composite of death, nonfatal myocardial infarction, revascularization, and significant angina) occurred in 24 patients (angiography-guided) and 23 patients (QFR-guided; P = 0.637, HR = 1.16 [0.63-2.15]). None of its components was different between groups. DISCUSSION: QFR guidance based on analysis of images from the primary intervention was not associated with a difference in the rate of non-culprit lesion staged revascularization nor in the 12-month incidence of clinical events in patients with acute coronary syndromes and multivessel disease. TRIAL REGISTRATION NUMBER: ClinicalTrials.gov Registry (NCT04808310).

Comparison of interventional treatment options for coronary calcified nodules: A sub-analysis of the ROTA.shock trial.

BACKGROUND: The optimal treatment for coronary calcified nodules (CNs) is still unclear. The aim of this study was to compare the modification of these lesions by coronary intravascular lithotripsy (IVL) and rotational atherectomy (RA) using optical coherence tomography (OCT). METHODS: ROTA.shock was a 1:1 randomized, prospective, double-arm multi-center non-inferiority trial that compared the use of IVL and RA with percutaneous coronary intervention (PCI) in severely calcified lesions. In 19 of the patients out of this study CNs were detected by OCT in the target lesion and were treated by either IVL or RA. RESULTS: The mean angle of CNs was significantly larger in final OCT scans than before RA (92 ± 17° vs. 68 ± 7°; p = 0.01) and IVL (89 ± 18° vs. 60 ± 10°; p = 0.03). The CNs were thinner upon final scans than in initial native scans (RA: 17.8 ± 7.8 mm vs. 38.6 ± 13.1 mm; p = 0.02; IVL: 16.5 ± 9.0 mm vs. 37.2 ± 14.3 mm; p = 0.02). Nodule volume did not differ significantly between native and final OCT scans (RA: 0.66 ± 0.12 mm3 vs. 0.61 ± 0.33 mm3; p = 0.68; IVL: 0.64 ± 0.19 mm3 vs. 0.68 ± 0.22 mm3; p = 0.74). Final stent eccentricity was high with 0.62 ± 0.10 after RA and 0.61 ± 0.09 after IVL. CONCLUSION: RA or IVL are unable to reduce the volume of the calcified plaque. CN modulation seems to be mainly induced by the stent implantation and not by RA or IVL.

Diseases of the Coronary Microcirculation: Diagnosis and Treatment.

BACKGROUND: Coronary microvascular dysfunction (CMD) comprises a variety of pathogenic mechanisms that impair the microcirculation of the heart. Clinical studies have shown that 30-50% of patients suffering from myocardial ischemia without significant coronary artery stenosis have CMD. The disease is associated with ele - vated mortality and poor quality of life. Whenever a patient presents with symptoms of angina pectoris and no underlying disease is detected by the usual methods, CMD should be considered a possible cause. METHODS: This review is based on publications retrieved by a selective search in PubMed and on current international guidelines and recommendations of specialty societies. RESULTS: The diagnosis of CMD is based on objective evidence of a microvascular origin of symptoms. The guidelines contain a class IIa recommendation for invasive coronary flow reserve and microvascular resistance measurements. Noninvasive tests such as positron emission tomography and cardiac magnetic resonance imaging are less accurate and are given a class IIb recommendation. No highquality therapeutic trials are available to date, and the treatment of CMD is thus based on that of chronic coronary syndrome. Lifestyle modification is performed to reduce risk factors. Patients with an abnormal coronary flow reserve or elevated microvascular resistance can be treated with an ACE inhibitor or angiotensin receptor blocker. Beta-blockers and calcium channel antagonists can relieve angina pectoris. Statins lower the LDL level and have positive pleiotropic effects. First-line treatment can be supplemented with further medications. CONCLUSION: Approximately 25% of patients with CMD have symptoms that do not respond to intensive treatment with the currently available modalities. New treatments, including interventional therapies, are being studied. Their long-term benefit remains to be assessed and compared to that of the existing methods.

Comparison of Coronary Intravascular Lithotripsy and Rotational Atherectomy in the Modification of Severely Calcified Stenoses.

Debulking techniques are often necessary for successful lesion preparation in percutaneous coronary intervention. The aim of this study was to compare plaque modification of severely calcified lesions by coronary intravascular lithotripsy (IVL) with that of rotational atherectomy (RA) using optical coherence tomography (OCT). ROTA.shock was a 1:1 randomized, prospective, double-arm, multicenter noninferiority trial designed to compare final minimal stent area after IVL with RA for lesion preparation in percutaneous coronary interventional treatment of severely calcified lesions. On the basis of OCT acquired before and immediately after IVL or RA in 21 of the 70 patients included, we performed a detailed analysis of the modification of the calcified plaque. After RA and IVL, calcified plaque fractures were present in 14 of the patients (67%), with a significantly greater number of fractures after IVL (3.23 ± 0.49) than after RA (1.67 ± 0.52; p < 0.001). Plaque fractures after IVL were longer than after RA (IVL: 1.67 ± 0.43 mm vs RA: 0.57 ± 0.55 mm; p = 0.01), resulting in a greater total volume of the fractures (IVL: 1.47 ± 0.40 mm3 vs RA: 0.48 ± 0.27 mm3; p = 0.003). Use of RA was associated with a greater acute lumen gain than was use of IVL (RA: 0.46 ± 0.16 mm2 vs IVL: 0.17 ± 0.14 mm2; p = 0.03). In conclusion, we were able to show differences in plaque modification of calcified coronary lesions by OCT: although RA leads to a greater acute lumen gain, IVL induces more and longer fractures of the calcified plaque.