The management of non-culprit coronary lesions in patients with acute coronary syndrome

About 50% of patients diagnosed with ST-segment elevation myocardial infarction have multivessel disease on coronary angiography. Recent evidence has shown that a staged percutaneous coronary intervention (PCI) strategy of non-culprit lesions, achieving complete revascularization, significantly reduces the rate of recurrent cardiovascular events compared with a PCI strategy limited to culprit lesion. Although functional evaluation of intermediate coronary stenoses by functional flow reserve (FFR) or instantaneous wave-free ratio (iFR) is widely used to detect residual myocardial ischaemia, the reliability of the study of non-culprit lesions in the acute phase of heart attack is controversial. On the other hand, the excess of new events in patients with acute coronary syndrome in whom PCI was deferred on the basis of FFR/iFR compared to patients with stable CAD could be due to both an inadequate functional evaluation and an intrinsic higher risk, related to the presence of untreated vulnerable plaques. In this context, intra-coronary imaging has shown that the presence of vulnerability features in non-culprit plaques is associated with an increased rate of ischaemic recurrence

Optimized treatment of ST-elevation myocardial infarction: the unmet need to target coronary microvascular obstruction as primary treatment goal to further improve prognosis

Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction

Patients with acute myocardial infarction and non-obstructive coronary arteries: Safety and prognostic relevance of invasive coronary provocative tests

Functional alterations of epicardial coronary arteries or coronary microcirculation represent a frequent cause of myocardial infarction and non-obstructive coronary arteries (MINOCA). We aimed at assessing the prognostic value of intracoronary provocative tests in patients presenting with MINOCA and in which other causes of MINOCA have been excluded. Methods and results We prospectively evaluated patients with a diagnosis of MINOCA, excluding patients with aetiologies other than suspected coronary vasomotor abnormalities. Immediately after coronary angiography, an invasive provocative test using acetylcholine or ergonovine was performed. The incidence of death from any cause, cardiac death, and recurrence of acute coronary syndrome (ACS) was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). We enrolled 80 consecutive patients [mean age 63.0±10.7 years, 40 (50%) male]. Provocative test was positive in 37 (46.2%) patients without any complication. Among patients with a positive test, epicardial spasm was detected in 24 (64.9%) patients and microvascular spasm in 13 (35.1%) patients. After a median follow-up of 36.0 (range 12.0-60.0)months, patients with a positive test had a significantly higher occurrence of death from any cause [12 (32.4%) vs. 2 (4.7%); P= 0.002], cardiac death [7 (18.9%) vs. 0 (0.0%); P= 0.005], and readmission for ACS [10 (27.0%) vs. 3 (7.0%); P= 0.015] as well as a worse angina status as assessed by SAQ [Seattle score: 88.0 (33.0-100.0) vs. 100.0 (44.0-100.0); P = 0.001] when compared with patients with a negative test. Conclusions We demonstrate that in patients presenting with MINOCA and suspected coronary vasomotor abnormalities, a positive provocative test for spasm is safe and identifies a high-risk subset of patients

Cardiac magnetic resonance predictors of left ventricular remodelling following acute ST elevation myocardial infarction: The VavirimS study

Left ventricular (LV) remodelling (REM) ensuing after ST-elevation myocardial infarction (STEMI), has typically been studied by echocardiography, which has limitations, or cardiac magnetic resonance (CMR) in early phase that may overestimate infarct size (IS) due to tissue edema and stunning. This prospective, multicenter study investigated LV-REM performing CMR in the subacute phase, and 6 months after STEMI

40. Optical coherence tomography correlates of complex lesions evaluated by coronary angiography in patients with acute coronary syndromes

Plaque rupture (PR) and superimposed thrombosis have been shown as the most frequent underlying substrate in acute coronary syndromes (ACS). Coronary angiography is a luminogram that is not able to define in-vivo features of the culprit plaques. The aim of the study was to use optical coherence tomography (OCT) to investigate the pathology underlying complex (CL) and non-complex angiographic lesions (NCL). Methods: We retrospectively enrolled 107 ACS patients admitted to our institution; 83 with Non-ST elevation ACS (NSTE-ACS) and 24 with ST-elevation myocardial infarction (STEMI). Coronary angiography was performed and culprit lesions were classified according to Ambrose criteria into NCL (n = 47) and CL (n = 60). In STEMI patients, angiographic and OCT analysis were performed after mechanical thrombus aspiration. OCT analysis of these culprit lesion was performed to identify plaque morphology; either PR or intact fibrous cap (IFC), as well as the presence of superimposed thrombosis, lipid rich plaque, thin cap fibroatheroma (TCFA), and minimal lumen area (MLA). Results: OCT analysis showed that 58 lesions (54.2%) were classified as PR and 48 lesions (44.9%) were associated with thrombi. Lipid rich plaques were identified in 62 culprit plaques (57.9%). PR, intracoronary thrombi, lipid rich plaques and thin cap fibroatheroma (TCFA) were more frequent in CL compared with NCL (71.7% vs 31.9%, 63.3% vs 21.3%, 71.7% vs 40.4% and 46.7% vs 21.3% respectively). PR (31.9%) with superimposed thrombus (21.3%) may be also detected in NCL. In STEMI patients, there was no significant difference regarding OCT plaque features between NCL and CL. Conclusion: In conclusion, OCT demonstrates PR and thrombosis in the majority of ACS patients presenting with CL. Of note, one third of NCL has PR and thrombosis by OCT. In STEMI, coronary angiography is of limited utility in identifying PR by means of CL and should be implemented with OCT to tailor future therapies