Procedural outcomes of chronic total occlusion percutaneous coronary interventions in patients with acute kidney injury.

BACKGROUND: The prognostic impact of contrast-associated acute kidney injury (CA-AKI) in patients undergoing chronic total occlusion (CTO) percutaneous coronary intervention (PCI) remains underestimated. METHODS: We examined 2707 consecutive procedures performed in a referral CTO center between 2015 and 2019. CA-AKI was defined as an increase in serum creatinine ≥ 0.3 mg/dL or ≥ 50% within 48 h post-PCI. Primary endpoints were in-hospital major adverse cardiac and cerebrovascular events (MACCE, composite of all-cause death, myocardial infarction, target vessel revascularization, stroke) and at one year of follow-up. RESULTS: The overall incidence of CA-AKI was 11.5%. Technical success was comparable (87.2% vs. 90.5%, p = 0.056) whereas procedural success was lower in the CA-AKI group (84.3% vs. 89.7%, p = 0.004). Overall in-hospital MACCE was 1.3%, and it was similar in patients with and without CA-AKI (1.6% vs. 1.3%, p = 0.655); however, the rate of pericardial tamponade requiring pericardiocentesis was significantly higher in patients with CA-AKI (2.2% vs. 0.5%, p = 0.001). In multivariate analysis, CA-AKI was not independently associated with higher risk for in-hospital MACCE (adjusted odds ratio [OR] 1.34, 95% confidence intervals [CI] 0.45-3.19, p = 0.563). At a median follow-up time of 14 months (interquartile range [IQR], 11 to 35 months), one-year MACCE was significantly higher in patients with vs. without CA-AKI (20.8% vs. 12.8%, p < 0.001), and CA-AKI increased the risk for one-year MACCE (adjusted hazard ratio [HR] 1.46, 95% CI 1.07-1.95, p = 0.017) following CTO PCI. CONCLUSIONS: CA-AKI in patients undergoing CTO PCI occurs in approximately one out of 10 patients. Our study highlights that patients developing CA-AKI are at increased risk for long-term MACCE.

Planned versus unplanned rotational atherectomy for plaque modification in severely calcified coronary lesions.

BACKGROUND: Evidence on the optimal timing of RA is scarce, although increased periprocedural complications for unplanned procedures have been reported. AIMS: To compare planned versus unplanned use of rotational atherectomy (RA) for plaque modification in patients with severely calcified coronary lesions. METHODS: Procedural and 1-year follow-up data of planned (n = 562 lesions in 448 vessels of 416 patients) and unplanned (n = 490 lesions in 435 vessels of 403 patients) RA between 2008 and 2020 were analyzed using the propensity score methods. The primary composite endpoint was target lesion failure (TLF), defined as cardiovascular death (CVD), target vessel myocardial infarction (TVMI), or target lesion revascularization (TLR). RESULTS: Angiographic success was > 99% in both groups. Fluoroscopy time and contrast volume were significantly lower in planned RA (p < 0.001). Periprocedural complications including slow-flow, coronary dissection, and MI occurred in 4.8% after planned, and in 5.7% after unplanned RA. TLF occurred in 18.5% after planned, and in 14.7% after unplanned RA. Weighted subdistribution hazard ratios for TLFs revealed an unfavorable 1-year outcome for planned RA (sHR 1.62 [1.07-2.45], p = 0.023), which was driven by TLR (sHR 2.01 [1.18-3.46], p = 0.011), but not by CVD, or TVMI. No differences were observed in all-cause mortality. CONCLUSIONS: Unplanned RA was associated with favorable outcome when compared to planned RA. Thus, RA can safely be reserved for lesions that prove untreatable by conventional means. Randomized and prospective trials are needed to evaluate a predominant use of rotational atherectomy as a bailout strategy in the future.

Prevalence and Causes of Myocardial Infarction with Non-Obstructive Coronary Arteries in a Contemporary Cohort of Patients with Suspected Myocardial Infarction.

BACKGROUND: A significant proportion of patients presenting with acute myocardial infarction (MI) has no coronary obstruction at coronary angiography and no other obvious non-coronary pathophysiology causing MI. These patients are classified as MI with non-obstructive coronary arteries (MINOCA). Data on incidence and predictors of MINOCA are still limited. METHODS: This study enrolled patients presenting symptoms suggestive of MI and undergoing a comprehensive cardiac work-up including an early invasive strategy. Patients with non-obstructive coronary arteries and without other obvious reasons for MI were scheduled for further work-up including magnetic resonance or intraluminal imaging. MINOCA was diagnosed according to the current European Society of Cardiology guidelines. RESULTS: From the 1532 patients enrolled, 730 had available coronary imaging and 546 were diagnosed with MI. No significant coronary obstructions were found in 117 patients with MI. After the exclusion of 6 patients with acute myocarditis or takotsubo-syndrome as well as 88 with type II MI, 23 patients were diagnosed with MINOCA (4% of all MIs). Among these 23 patients, the most common etiology of MINOCA was thromboembolic events followed by coronary spasm. Female sex, the absence of hypercholesterolemia, and a normal left-ventricular ejection fraction were independently predictive for MINOCA compared to patients with other causes of MI. CONCLUSION: More than 20% of patients presenting with acute MI showed no significant coronary obstruction. About 4% of these patients were diagnosed with MINOCA. Female sex, a lower cardiovascular risk profile, and normal left-ventricular function were predictive for MINOCA.

Evaluation of a 1-hour troponin algorithm for diagnosing myocardial infarction in high-risk patients admitted to a chest pain unit: the prospective FAST-MI cohort study.

OBJECTIVE: This study sought to evaluate the diagnostic performance of the 1-hour troponin algorithm for diagnosis of myocardial infarction (MI) without persistent ST-segment elevations (non-ST-segment MI (NSTEMI)) in a cohort with a high prevalence of MI. This algorithm recommend by current guidelines was previously developed in cohorts with a prevalence of MI of less than 20%. DESIGN: Prospective cohort study from November 2015 until December 2016. SETTING: Dedicated chest pain unit of a single referral centre. PARTICIPANTS: Consecutive patients with suspected MI were screened. Patients with subacute symptoms lasting more than 24 hours, new ST-segment elevations at presentation, or an already diagnosed or ruled-out acute MI were excluded. All enrolled patients (n=1317) underwent a full clinical assessment and measurements of high-sensitivity troponin, and were scheduled for an early invasive strategy if clinically indicated. MAIN OUTCOME MEASURES: Final diagnosis of MI according to the Fourth Universal Definition of MI. RESULTS: The prevalence of NSTEMI in the present cohort was 36.9%. The sensitivity for rule-out of MI was 99.8%. The specificity for rule-in of MI was found to be 94.3%. However, in 35.7% of patients neither rule-in nor rule-out was possible. In 51.4% of patients diagnosed with MI, a primary non-coronary reason for MI was found (type 2 MI). Different receiver operating characteristic-curve derived cut-offs for troponin and its dynamics did not provide a sufficient differentiation between type 1 and 2 MI for clinical decision making (negative predictive value for rule-out of type 1 MI <70%). CONCLUSIONS: The 1-hour diagnosis algorithm for patients with suspected NSTEMI can accurately diagnose acute MI in high-risk cohorts. However, discrimination between patients needing an early invasive strategy or not is limited. TRIAL REGISTRATION NUMBER: DRKS00009713.

Sphingosine 1-Phosphate Produced by Sphingosine Kinase 2 Intrinsically Controls Platelet Aggregation In Vitro and In Vivo.

RATIONALE: Platelets are known to play a crucial role in hemostasis. Sphingosine kinases (Sphk) 1 and 2 catalyze the conversion of sphingosine to the bioactive metabolite sphingosine 1-phosphate (S1P). Although platelets are able to secrete S1P on activation, little is known about a potential intrinsic effect of S1P on platelet function. OBJECTIVE: To investigate the role of Sphk1- and Sphk2-derived S1P in the regulation of platelet function. METHODS AND RESULTS: We found a 100-fold reduction in intracellular S1P levels in platelets derived from Sphk2(-/-) mutants compared with Sphk1(-/-) or wild-type mice, as analyzed by mass spectrometry. Sphk2(-/-) platelets also failed to secrete S1P on stimulation. Blood from Sphk2-deficient mice showed decreased aggregation after protease-activated receptor 4-peptide and adenosine diphosphate stimulation in vitro, as assessed by whole blood impedance aggregometry. We revealed that S1P controls platelet aggregation via the sphingosine 1-phosphate receptor 1 through modulation of protease-activated receptor 4-peptide and adenosine diphosphate-induced platelet activation. Finally, we show by intravital microscopy that defective platelet aggregation in Sphk2-deficient mice translates into reduced arterial thrombus stability in vivo. CONCLUSIONS: We demonstrate that Sphk2 is the major Sphk isoform responsible for the generation of S1P in platelets and plays a pivotal intrinsic role in the control of platelet activation. Correspondingly, Sphk2-deficient mice are protected from arterial thrombosis after vascular injury, but have normal bleeding times. Targeting this pathway could therefore present a new therapeutic strategy to prevent thrombosis.