Objectives. The study evaluated the correlation between baseline SYNTAX Score, Residual SYNTAX Score, and SYNTAX Revascularization Index and long-term outcomes in ST-elevation myocardial infarction (STEMI) patients with primary percutaneous coronary intervention (PCI) on an unprotected left main coronary artery lesion (UPLMCA). Background. Previous studies on primary PCI in UPLMCA have identified cardiogenic shock, TIMI 0/1 flow, and cardiac arrest, as prognostic factors of an unfavourable outcome, but the complexity of coronary artery disease and the extent of revascularization have not been thoroughly investigated in these high-risk patients. Methods. 30-day, 1-year, and long-term outcomes were analyzed in a cohort of retrospectively selected, 81 consecutive patients with STEMI, and primary PCI on UPLMCA. Results. Cardiogenic shock (p=0.001), age (p=0.008), baseline SYNTAX Score II (p=0.006), and SYNTAX Revascularization Index (p=0.046) were independent mortality predictors at one-year follow-up. Besides cardiogenic shock (HR 3.28, p<0.001), TIMI 0/1 flow (HR 2.17, p=0.021) and age (HR 1.03, p=0.006), baseline SYNTAX Score II (HR 1.06, p=0.006), residual SYNTAX Score (HR 1.03, p=0.041), and SYNTAX Revascularization Index (HR 0.9, p=0.011) were independent predictors of mortality at three years of follow-up. In patients with TIMI 0/1 flow, the presence of Rentrop collaterals was an independent predictor for long-term survival (HR 0.24; p=0.049). Conclusions. In this study, the complexity of coronary artery disease and the extent of revascularization represent independent mortality predictors at long-term follow-up.

In the setting of acute myocardial infarction, flow restoration in the culprit epicardial coronary artery is not synonymous with efficient reperfusion. Microvascular obstruction occurs in 50% of cases and represents a predictor of a long-term unfavorable outcome. Its prevalence has remained constant in recent years despite various treatment attempts. However, the success of targeted therapies could be mainly a problem of timing. Recent data bring evidence with regard to the role of pre-procedural distal embolization and highlight the relation between distal embolism, microvascular obstruction and intramyocardial inflammation. As a result, early detection of microvascular injury represents the first step in the development of targeted, individualized therapeutic approaches. In this context, the identification of new invasive surrogate parameters for the timely assessment and quantification of microvascular obstruction in the catheterization laboratory has become an important subject of current research. Among these, coronary wedge pressure is the most practical and revealing in the setting of primary percutaneous coronary intervention. It may offer comprehensive details on the mechanisms of microvascular injury and may therefore offer guidance for appropriate treatment selection.

The aim of this study was to investigate the relationship between coronary wedge pressure (CWP), measured as a marker of pre-procedural microvascular obstruction, and left ventricular remodelling in high-risk ST-segment elevation myocardial infarction (STEMI) patients. Pre-revascularization CWP was measured in 25 patients with high-risk anterior STEMI. Left ventricular volumes and ejection fraction were echocardiographically measured at discharge and at follow-up. A 20% increase in left ventricular volumes was used to define remodelling. Patients with CWP ≤ 38 mmHg were characterized by late ventricular remodelling. Patients with CWP > 38 mmHg developed a progressive remodelling process which was associated with a significant 60 months increase in left ventricular volumes (P = 0.01 for end-systolic volume and 0.03 for end-diastolic volume) and a significant decrease in left ventricular ejection fraction (P = 0.05). A significant increase in both left ventricular end-systolic (P = 0.009) and end-diastolic volume (P = 0.02) from baseline to 60 months follow-up was recorded in patients with extracted thrombus length ≥2 mm. Pre-revascularization elevated CWP was associated with increased left ventricular volumes and decreased ejection fraction at long-term follow-up. CWP was a predictor of severe left ventricular enlargement, besides extracted thrombus quantity.

Background: Patients with ST-segment elevation myocardial infarction (STEMI) and primary percutaneous coronary intervention (PPCI) on a left main culprit lesion have very high mortality rates. The interaction of chronic kidney disease (CKD) with such a catastrophic acute event on the background of their highly complex atherosclerotic lesions is not well established. Therefore, we sought to evaluate in these patients the influence of the estimated glomerular filtration rate (eGFR) on short- and long-term mortality. Methods: We retrospectively analyzed renal function in 81 patients with STEMI and PPCI on a left main culprit lesion from two tertiary centers. Results: Patients were divided in two groups according to an eGFR cut-off of 60 mL/min/1.73 m²: 40 patients with CKD and 41 without CKD. Patients with renal failure were older, had more diabetes, and had experienced more frequent myocardial infarction MIs. CKD patients had a higher baseline-SYNTAX score (p = 0.015), higher residual-SYNTAX score (p < 0.001), and lower SYNTAX revascularization index-SRI (p = 0.003). Mortality at 30-day, 1-year, and 3-year follow-ups were not significantly different between the two groups. However, when analyzed as a continuous variable, eGFR emerged as a predictor of 1-year mortality, both in univariate analysis (OR = 0.97, 95% CI: 0.95–0.99, p = 0.005) and in multivariate analysis, after adjusting for cardiogenic shock and Thrombolysis in Myocardial Infarction TIMI 0/1 flow (OR = 0.975, 95% CI: 0.95–0.99, p = 0.021). Conclusions: In STEMI with PPCI on a left main culprit lesion, renal failure was associated with more complex coronary lesions and less complete revascularization, and turned out to be an independent predictor of mortality at 1-year follow-up.

BACKGROUND: Atherosclerotic renal artery stenosis is a risk factor for cardiovascular death. Observational studies support the benefit of renal revascularization on outcomes in patients with high-risk clinical manifestations. In this context, we evaluated the factors associated with long-term mortality after renal artery stenting in patients with severe renal artery stenosis, impaired kidney function, and/or uncontrolled hypertension. METHODS: The medical records of patients undergoing renal artery stenting between 2004 and 2014 were extracted. Blood pressure and creatinine were recorded at baseline, 24 hours poststenting and in the 1-month to 1-year interval that followed revascularization. Long-term follow-up was performed in March 2020. RESULTS: The cohort consisted of 65 patients. Median follow-up was 120 months. In the first year after stenting, less patients had chronic kidney disease (CKD) class 3b–5 as compared with baseline (35.3% vs. 56.9%, P = 0.01). The number of patients with controlled blood pressure after revascularization increased with 69.2% (P < 0.001). Long-term all-cause mortality reached 44.6%. Age (odds ratio (OR) 1.1; 95% confidence interval (CI) 1.0–1.2; P = 0.01), male gender (OR 7.9; 95% CI 1.9–43.5; P = 0.008), poststenting CKD class 3b–5 (OR 5.8; 95% CI 1.5–27.9; P = 0.01), and postrevascularization uncontrolled hypertension (OR 8.9; 95% CI 1.7–63.5; P = 0.01) were associated with long-term mortality independent of diabetes mellitus and coronary artery disease. CONCLUSIONS: Improved CKD class and blood pressure were recorded in the first year after renal artery stenting in patients with severe renal artery stenosis and high-risk clinical manifestations. The lack of improvement in kidney function and blood pressure was independently associated with long-term mortality.

Human diseases arise in a complex ecosystem composed of disease mechanisms and the whole-body state. However, the precise nature of the whole-body state and its relations with disease remain obscure. Here we map similarities among clinical parameters in normal physiological settings, including a large collection of metabolic, hemodynamic, and immune parameters, and then use the mapping to dissect phenotypic states. We find that the whole-body state is faithfully represented by a quantitative two-dimensional model. One component of the whole-body state represents ‘metabolic syndrome’ (MetS) – a conventional way to determine the cardiometabolic state. The second component is decoupled from the classical MetS, suggesting a novel ‘non-classical MetS’ that is characterized by dozens of parameters, including dysregulated lipoprotein parameters (e.g. low free cholesterol in small high-density lipoproteins) and attenuated cytokine responses of immune cells to ex vivo stimulations. Both components are associated with disease, but differ in their particular associations, thus opening new avenues for improved personalized diagnosis and treatment. These results provide a practical paradigm to describe whole-body states and to dissect complex disease within the ecosystem of the human body.