Differences between cardiogenic shock related to acute decompensated heart failure and acute myocardial infarction.

AIMS: The present analysis from the multicentre prospective Altshock-2 registry aims to better define clinical features, in-hospital course, and management of cardiogenic shock complicating acutely decompensated heart failure (ADHF-CS) as compared with that complicating acute myocardial infarction (AMI-CS). METHODS AND RESULTS: All patients with AMI-CS or ADHF-CS enrolled in the Altshock-2 registry between March 2020 and February 2022 were selected. The primary objective was the characterization of ADHF-CS patients as compared with AMI-CS. In-hospital length of stay and mortality were secondary endpoints. One-hundred-ninety of the 238 CS patients enrolled in the aforementioned period were considered for the present analysis: 101 AMI-CS (80% ST-elevated myocardial infarction and 20% non-ST-elevated myocardial infarction) and 89 ADHF-CS. As compared with AMI-CS, ADHF-CS patients were younger [63 (IQR 59-76) vs. 67 (IQR 54-73) years, P = 0.01], but presented with higher creatinine [1.6 (IQR 1.0-2.6) vs. 1.2 (IQR 1.0-1.4) mg/dL, P < 0.001], bilirubin [1.3 (IQR 0.9-2.3) vs. 0.6 (IQR 0.4-1.1) mg/dL, P = 0.01], and central venous pressure values [14 mmHg (IQR 8-12) vs. 10 mmHg (IQR 7-14),P = 0.01]. Norepinephrine was the most common catecholamine used in AMI-CS (79.3%), whereas epinephrine was used more commonly in ADHF-CS (65.5%); 75.8% vs. 46.6% received a temporary mechanical support in AMI-CS and ADHF-CS, respectively (P < 0.001). Length of hospital stay was longer in the latter [28 (IQR 13-48) vs. 17 (IQR 9-29) days, P = 0.001]. Heart replacement therapies were more frequently used in the ADHF-CS group (heart transplantation 13.5% vs. 0% and left ventricular assist device 11% vs. 2%, P < 0.01 and 0.01, respectively). In-hospital mortality was 41.1% (38.6% AMI-CS vs. 43.8% ADHF-CS, P = 0.5). CONCLUSIONS: ADHF-CS is characterized by a higher prevalence of end-organ and biventricular dysfunction at presentation, a longer hospital length of stay, and higher need of heart replacement therapies when compared with AMI-CS. In-hospital mortality was similar between the two aetiologies. Our data warrant development of new management protocols focused on CS aetiology.

Transcatheter mitral valve replacement: there is still work to be done.

Transcatheter mitral valve replacement (TMVR) is a novel therapeutic option for patients with severe mitral regurgitation (MR) at high or prohibitive surgical risk. Most TMVR technologies under investigation use either a trans-apical or a trans-septal approach via dedicated multistep anchoring systems. Transcatheter mitral valve replacement offers several potential advantages over transcatheter repair, notably a greater and more sustained MR reduction. At the same time, significant engineering challenges and potential disadvantages must be acknowledged. Preclinical and clinical studies have shown promising results, demonstrating TMVR feasibility. Nevertheless, further development, testing, and trials are needed before considering TMVR as a definitive therapeutic option for MR in a wide range of anatomical scenarios.

A case of myopericarditis recurrence after third dose of BNT162b2 vaccine against SARS-CoV-2 in a young subject: link or causality?

The rate of post-vaccine myocarditis is being studied from the beginning of the massive vaccination campaign against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although a direct cause-effect relationship has been described, in most cases, the vaccine pathophysiological role is doubtful. Moreover, it is not quite as clear as having had a previous myocarditis could be a risk factor for a post-vaccine disease relapse. A 27-year-old man presented to the emergency department for palpitations and pericardial chest pain radiated to the upper left limb, on the 4th day after the third dose of BNT162b2 vaccine. He experienced a previous myocarditis 3 years before, with full recovery and no other comorbidities. Electrocardiogram showed normal atrioventricular conduction, incomplete right bundle branch block, and diffuse ST-segment elevation. A cardiac echo showed lateral wall hypokinesis with preserved ejection fraction. Troponin-T was elevated (160 ng/L), chest X-ray was normal, and the SARS-CoV-2 molecular buffer was negative. High-dose anti-inflammatory therapy with ibuprofen and colchicine was started; in the 3rd day high-sensitivity Troponin I reached a peak of 23000 ng/L. No heart failure or arrhythmias were observed. A cardiac magnetic resonance was performed showing normal biventricular systolic function and abnormal tissue characterization suggestive for acute non-ischaemic myocardial injury (increased native T1 and T2 values, increased signal intensity at T2-weighted images and late gadolinium enhancement, all findings with matched subepicardial distribution) at the level of mid to apical septal, anterior, and anterolateral walls. A left ventricular electroanatomic voltage mapping was negative (both unipolar and bipolar), while the endomyocardial biopsy showed a picture consistent with active myocarditis. The patient was discharged in good clinical condition, on bisoprolol 1.25 mg, ramipril 2.5 mg, ibuprofen 600 mg three times a day, colchicine 0.5 mg twice a day. We presented the case of a young man with history of previous myocarditis, admitted with a non-complicated acute myopericarditis relapse occurred 4 days after SARS-CoV-2 vaccination (3rd dose). Despite the observed very low incidence of cardiac complications following BNT162b2 administration, and the lack of a clear proof of a direct cause-effect relationship, we think that in our patient this link can be more than likely. In the probable need for additional SARS-CoV-2 vaccine doses in the next future, studies addressing the risk-benefit balance of this subset of patient are warranted. We described a multidisciplinary management of a case of myocarditis recurrence after the third dose of SARS-CoV-2 BNT162b2 vaccine.

Acute kidney injury and in-hospital mortality in patients with ST-elevation myocardial infarction of different age groups.

BACKGROUND: Acute kidney injury (AKI) is a well-known complication of ST-elevation acute myocardial infarction (STEMI) with an adverse impact on prognosis. Since AKI develops more frequently in elderly patients, we hypothesized that its higher incidence in older STEMI patients might explain their increased in-hospital mortality. We assessed the relationship between AKI and in-hospital mortality in patients with STEMI of different age groups. METHODS: We retrospectively evaluated 5136 STEMI patients treated with primary percutaneous coronary intervention (pPCI). We defined AKI as ≥0.5 mg/dl creatinine increase in the first 72 h. Patients were grouped according to age (<75 [n = 4040] or ≥ 75 [n = 1096] years). The primary endpoint was in-hospital mortality. RESULTS: The incidence of AKI was 7%. It was 4.6% in patients <75 years and 15.1% in those ≥75 years (P < 0.0001). The overall in-hospital mortality was 4%. It was 2.6% and 8.5% in patients younger and older than 75 years, respectively (P < 0.0001). It was higher in AKI than in non-AKI patients, both in the overall population (27% vs. 2%) and in the two age groups (25% vs. 2% and 29% vs. 5% in younger and older patients, respectively; P < 0.0001). The adjusted odds ratio of in-hospital mortality associated with AKI progressively decreased in parallel with increasing age decades (from 24.7 [95% CI 11.2-54.1] in patients <65 years to 3.9 [95% CI 1.6-9.7] in those >85 years). CONCLUSIONS: In STEMI patients treated with pPCI, AKI incidence and in-hospital mortality steadily increase with age. However, the prognostic impact of AKI is progressively reduced as age increases.

ST-Segment Elevation Acute Myocardial Infarction Complicated by Cardiogenic Shock: Early Predictors of Very Long-Term Mortality.

BACKGROUND: Cardiogenic shock (CS) is the leading cause of in-hospital mortality in ST-segment elevation myocardial infarction (STEMI). Only limited data are available on the long-term outcome of STEMI patients with CS undergoing contemporary treatment. We aimed to investigate long-term mortality and its predictors in STEMI patients with CS and to develop a risk score for long-term mortality prediction. METHODS AND RESULTS: We retrospectively included 465 patients with STEMI complicated by CS and treated with primary angioplasty and intra-aortic balloon pump between 2005 and 2018. Long-term mortality, including both in-hospital mortality and all-cause mortality following discharge from the index hospitalization, was the primary endpoint. The long-term mortality (median follow-up 4 (2.0-5.2) years) was 60%, including in-hospital mortality (34%). At multivariate analysis, independent predictors of long-term mortality were age (HR 1.41, each 10-year increase), admission left ventricular ejection fraction (HR 1.51, each 10%-unit decrease) and creatinine (HR 1.28, each mg/dl increase), and acute kidney injury (HR 1.81). When these predictors were pooled together, the area under the curve (AUC) for long-term mortality was 0.80 (95% CI 0.75-0.84). Using the four variables, we developed a risk score with a mean (cross-validation analysis) AUC of 0.79. When the score was applied to in-hospital mortality, its AUC was 0.79, and 0.76 when the score was applied to all-cause mortality following discharge. CONCLUSIONS: In STEMI patients with CS, the risk of death is still substantial in the years following the index event. A simple clinical score at the time of the index event accurately predicts long-term mortality risk.

Mitochondrial Biomarkers in Patients with ST-Elevation Myocardial Infarction and Their Potential Prognostic Implications: A Prospective Observational Study.

BACKGROUND: Mitochondrial biomarkers have been investigated in different critical settings, including ST-elevation myocardial infarction (STEMI). Whether they provide prognostic information in STEMI, complementary to troponins, has not been fully elucidated. We prospectively explored the in-hospital and long-term prognostic implications of cytochrome c and cell-free mitochondrial DNA (mtDNA) in STEMI patients undergoing primary percutaneous coronary intervention. METHODS: We measured cytochrome c and mtDNA at admission in 466 patients. Patients were grouped according to mitochondrial biomarkers detection: group 1 (-/-; no biomarker detected; n = 28); group 2 (-/+; only one biomarker detected; n = 283); group 3 (+/+; both biomarkers detected; n = 155). A composite of in-hospital mortality, cardiogenic shock, and acute pulmonary edema was the primary endpoint. Four-year all-cause mortality was the secondary endpoint. RESULTS: Progressively lower left ventricular ejection fractions (52 ± 8%, 49 ± 8%, 47 ± 9%; p = 0.006) and higher troponin I peaks (54 ± 44, 73 ± 66, 106 ± 81 ng/mL; p = 0.001) were found across the groups. An increase in primary (4%, 14%, 19%; p = 0.03) and secondary (10%, 15%, 23%; p = 0.02) endpoint rate was observed going from group 1 to group 3. The adjusted odds ratio increment of the primary endpoint from one group to the next was 1.65 (95% CI 1.04-2.61; p = 0.03), while the adjusted hazard ratio increment of the secondary endpoint was 1.55 (95% CI 1.12-2.52; p = 0.03). The addition of study group allocation to admission troponin I reclassified 12% and 22% of patients for the primary and secondary endpoint, respectively. CONCLUSIONS: Detection of mitochondrial biomarkers is common in STEMI and seems to be associated with in-hospital and long-term outcome independently of troponin.

A preprocedural risk score predicts acute kidney injury following primary percutaneous coronary intervention.

BACKGROUND: Reliable preprocedural risk scores for the prediction of Contrast-Induced Acute Kidney Injury (CI-AKI) following Percutaneous Coronary Intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) are lacking. Aim of this study was to derive and validate a preprocedural Risk Score in this setting. METHODS: Two prospectively enrolled patient cohorts were used for derivation and validation (n = 3,736). CI-AKI was defined as creatinine increase ≥0.5 mg/dl <72 h postpPCI. Odds ratios from multivariable logistic regression model were converted to an integer, whose sum represented the Risk Score. RESULTS: Independent CI-AKI predictors were: diabetes, Killip class II-III (2 points each), age > 75 years, anterior MI (3 points), Killip class IV (4 points), estimated GFR < 60 ml/min/1.73m2 (5 points). The Risk Score c-statistic was 0.84 in both cohorts. Compared with patients with Risk Score ≤ 4, the relative risks of CI-AKI among patients scoring 5-9 were 6.2 (derivation cohort) and 7.1 (validation cohort); among patients scoring ≥10, 19.8, and 21.4, respectively. CONCLUSIONS: Among STEMI patients, a simple preprocedural Risk Score accurately and reproducibly predicted the risk of CI-AKI, identifying » of patients with a seven-fold risk and 1/10 of patients with a 20-fold risk. This knowledge may help tailored strategies, including delaying revascularization of nonculprit vessels in patients at high risk of CI-AKI.

Impact of Glomerular Filtration Rate on the Incidence and Prognosis of New-Onset Atrial Fibrillation in Acute Myocardial Infarction.

BACKGROUND: Atrial fibrillation (AF) is a frequent complication of acute myocardial infarction (AMI) and is associated with a worse prognosis. Patients with chronic kidney disease are more likely to develop AF. Whether the association between AF and glomerular filtration rate (GFR) is also true in AMI has never been investigated. METHODS: We prospectively enrolled 2445 AMI patients. New-onset AF was recorded during hospitalization. Estimated GFR was estimated at admission, and patients were grouped according to their GFR (group 1 (n = 1887): GFR >60; group 2 (n = 492): GFR 60-30; group 3 (n = 66): GFR <30 mL/min/1.73 m2). The primary endpoint was AF incidence. In-hospital and long-term (median 5 years) mortality were secondary endpoints. RESULTS: The AF incidence in the population was 10%, and it was 8%, 16%, 24% in groups 1, 2, 3, respectively (p < 0.0001). In the overall population, AF was associated with a higher in-hospital (5% vs. 1%; p < 0.0001) and long-term (34% vs. 13%; p < 0.0001) mortality. In each study group, in-hospital mortality was higher in AF patients (3.5% vs. 0.5%, 6.5% vs. 3.0%, 19% vs. 8%, respectively; p < 0.0001). A similar trend was observed for long-term mortality in three groups (20% vs. 9%, 51% vs. 24%, 81% vs. 50%; p < 0.0001). The higher risk of in-hospital and long-term mortality associated with AF in each group was confirmed after adjustment for major confounders. CONCLUSIONS: This study demonstrates that new-onset AF incidence during AMI, as well as the associated in-hospital and long-term mortality, increases in parallel with GFR reduction assessed at admission.

Iron deficiency in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

BACKGROUND: Iron deficiency (ID) is a known co-morbidity and a potential therapeutic target in heart failure. Whether ID is frequent also in ST-segment elevation acute myocardial infarction (STEMI) patients and is associated with worse in-hospital outcomes has never been evaluated. METHODS: We defined ID as a serum ferritin < 100 µg/L or transferrin saturation < 20% at hospital admission. We assessed the association between ID and the primary endpoint (a composite of in-hospital mortality and Killip class ≥ 3). We explored the potential association between ID, circulating cell-free mitochondrial DNA (mtDNA), and cardiac magnetic resonance (CMR) parameters. RESULTS: Four-hundred-twenty STEMI patients undergoing primary percutaneous coronary intervention (pPCI) were included. Of them, 237 (56%) had ID. They had significantly higher admission high-sensitivity troponin and mtDNA levels as compared to non-ID patients (145 ±â€¯35 vs. 231 ±â€¯66 ng/L, P < 0.001; 917 [404-1748] vs. 1368 [908-4260] copies/µL; P < 0.003, respectively). A lower incidence of the primary endpoint (10% vs. 18%, P = 0.01) was observed in ID patients (adjusted OR 0.50 [95% CI 0.27-0.93]; P = 0.02). At CMR (n = 192), ID patients had a similar infarct size (21 ±â€¯18 vs. 21 ±â€¯19 g; P = 0.95), but a higher myocardial salvage index (0.56 ±â€¯0.30 vs. 0.43 ±â€¯0.27; P = 0.002), and a smaller microvascular obstruction extent (3.6 ±â€¯2.2 vs. 6.9 ±â€¯3.9 g; P < 0.001). CONCLUSIONS: Iron deficiency is frequent in STEMI patients, it is coupled with mitochondrial injury, and, paradoxically, with a better in-hospital outcome. This unexpected clinical result seems to be associated with a smaller myocardial reperfusion injury. The mechanisms underlying our findings and their potential clinical implications warrant further investigation.

High-Sensitivity C-Reactive Protein and Acute Kidney Injury in Patients with Acute Myocardial Infarction: A Prospective Observational Study.

Background. Accumulating evidence suggests that inflammation plays a key role in acute kidney injury (AKI) pathogenesis. We explored the relationship between high-sensitivity C-reactive protein (hs-CRP) and AKI in acute myocardial infarction (AMI). Methods. We prospectively included 2,063 AMI patients in whom hs-CRP was measured at admission. AKI incidence and a clinical composite of in-hospital death, cardiogenic shock, and acute pulmonary edema were the study endpoints. Results. Two-hundred-thirty-four (11%) patients developed AKI. hs-CRP levels were higher in AKI patients (45 ± 87 vs. 16 ± 41 mg/L; p < 0.0001). The incidence and severity of AKI, as well as the rate of the composite endpoint, increased in parallel with hs-CRP quartiles (p for trend <0.0001 for all comparisons). A significant correlation was found between hs-CRP and the maximal increase of serum creatinine (R = 0.23; p < 0.0001). The AUC of hs-CRP for AKI prediction was 0.69 (p < 0.001). At reclassification analysis, addition of hs-CRP allowed to properly reclassify 14% of patients when added to creatinine and 8% of patients when added to a clinical model. Conclusions. In AMI, admission hs-CRP is closely associated with AKI development and severity, and with in-hospital outcomes. Future research should focus on whether prophylactic renal strategies in patients with high hs-CRP might prevent AKI and improve outcome.

Extended dual antiplatelet therapy after acute myocardial infarction. Current evidence and future perspectives.

Patients with acute myocardial infarction (AMI) are at increased risk of recurrent ischemic events after hospital discharge, despite optimal medical therapy. Current practice guidelines strongly encourage the early assessment of the residual ischemic risk in post-AMI patients, in order to identify those who may benefit from a prolonged dual antiplatelet therapy. To this end, some scoring systems have been proposed. However, most scores were developed for patients with stable coronary artery disease undergoing percutaneous coronary intervention. Moreover, nearly all failed to be implemented in everyday clinical practice, probably because of the perceived complexity due to the large number of incorporated variables. Therefore, the identification of the ideal AMI patient who can benefit from a prolonged (beyond 1 year after the index event) dual antiplatelet therapy remains to be clarified, especially when the bleeding risk associated with such therapy is considered. In this review, we summarize the current evidence on the prolonged use of dual antiplatelet therapy after AMI, with a special focus on recent advances regarding the identification of high-risk patients who may derive a favorable net clinical benefit from such a therapeutic strategy.

Reduced Cardio-Renal Function Accounts for Most of the In-Hospital Morbidity and Mortality Risk Among Patients With Type 2 Diabetes Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction.

OBJECTIVE: ST-segment elevation myocardial infarction (STEMI) patients with type 2 diabetes mellitus (DM) have higher in-hospital mortality than those without. Since cardiac and renal functions are the main variables associated with outcome in STEMI, we hypothesized that this prognostic disparity may depend on a higher rate of cardiac and renal dysfunction in DM patients. RESEARCH DESIGN AND METHODS: We retrospectively analyzed 5,152 STEMI patients treated with primary angioplasty. Left ventricular ejection fraction (LVEF) and estimated glomerular filtration rate (eGFR) were evaluated at hospital admission. The primary end point was in-hospital mortality. A composite of in-hospital mortality, cardiogenic shock, and acute kidney injury was the secondary end point. RESULTS: There were 879 patients (17%) with DM. The incidence of LVEF ≤40% (30% vs. 22%), eGFR ≤60 mL/min/1.73 m2 (27% vs. 18%), or both (12% vs. 6%) was higher (P < 0.001 for all comparisons) in DM patients. In-hospital mortality was higher in DM patients than in non-DM patients (6.1% vs. 3.5%; P = 0.002), with an unadjusted odds ratio (OR) of 1.81 (95% CI 1.31-2.49; P < 0.001). However, DM was no longer associated with an increased mortality risk after adjustment for cardiac and renal function (OR 1.03, 95% CI 0.68-1.56; P = 0.89). A similar behavior was observed for the secondary end point, with an unadjusted OR for DM of 1.52 (95% CI 1.25-1.85; P < 0.001) and an OR after adjustment for cardiac and renal function of 1.07 (95% CI 0.85-1.36; P = 0.53). CONCLUSIONS: The study indicates that the increased in-hospital mortality and morbidity of DM patients with STEMI is mainly driven by their underlying cardio-renal dysfunction.

Treatment of refractory vasospastic angina complicated by acute pulmonary oedema with levosimendan: a case report.

BACKGROUND: Vasospastic angina (VA) is an important cause of chest pain and patients often have 3- to 6-month clusters of recurrent attacks, separated by relatively asymptomatic periods. During these episodes the resulting myocardial ischaemia can lead to clinical complications of different severity, including acute myocardial infarction, acute heart failure, and cardiogenic shock. The management of severe and recurrent VA attacks is challenging, and no specific recommendations exist in recent cardiologic guidelines on the pharmacological strategy (inotropic/vasopressor agents) to adopt for this acute clinical setting. CASE SUMMARY: We present a case of recurrent episodes of VA complicated by acute pulmonary oedema and cardiogenic shock despite maximal tolerated therapy (intravenous calcium antagonist and nitrates) that was successfully treated with levosimendan. DISCUSSION: Levosimendan rapidly reverted cardiogenic shock, acute pulmonary oedema, and mitral regurgitation caused by a refractory coronary spasm, contributing to persistent clinical stabilization. Further evidence and a longer follow-up are needed to support our observation on the efficacy of levosimendan in this specific clinical setting.

Experienced Use of Dexmedetomidine in the Intensive Care Unit: A Report of a Structured Consensus.

OBJECTIVE: Management of pain, agitation and delirium (PAD) remains to be a true challenge in critically ill patients. The pharmacological proprieties of dexmedetomidine (DEX) make it an ideal candidate drug for light and cooperative sedation, but many practical questions remain unanswered. This structured consensus from 17 intensivists well experienced on PAD management and DEX use provides indications for the appropriate use of DEX in clinical practice. METHODS: A modified RAND/UCLA appropriateness method was used. In four predefined patient populations, the clinical scenarios do not properly cope by the current recommended pharmacological strategies (except DEX), and the possible advantages of DEX use were identified and voted for agreement, after reviewing literature data. RESULTS: Three scenarios in medical patients, five scenarios in patients with acute respiratory failure undergoing non-invasive ventilation, three scenarios in patients with cardiac surgery in the early postoperative period and three scenarios in patients with overt delirium were identified as challenging with the current PAD strategies. In these scenarios, the use of DEX was voted as potentially useful by most of the panellists owing to its specific pharmacological characteristics, such as conservation of cognitive function, lack of effects on the respiratory drive, low induction of delirium and analgesia effects. CONCLUSION: DEX might be considered as a first-line sedative in different scenarios even though conclusive data on its benefits are still lacking.

Acute kidney injury after lung cancer surgery: Incidence and clinical relevance, predictors, and role of N-terminal pro B-type natriuretic peptide.

BACKGROUND: Acute kidney injury (AKI) frequently occurs in several medical and surgical settings, and it is associated with increased morbidity and mortality. In patients undergoing lung cancer surgery, AKI has not been fully investigated. We prospectively evaluated the incidence, clinical relevance, and risk factors of AKI in patients undergoing lung cancer surgery. Moreover, we estimated the accuracy of N-terminal pro-B-type natriuretic peptide (NT-proBNP) in the prediction of AKI. METHODS: Patients undergoing lung cancer surgery were included in the study. Plasma NT-proBNP was measured before and soon after surgery. Postoperative AKI was defined according to the Acute Kidney Injury Network (AKIN) classification. RESULTS: A total of 2179 patients were enrolled. Of them, 222 (10%) developed AKI and had a more complicated in-hospital clinical course (overall complication rate: 35% vs. 16%; P < 0.0001), and a longer hospital stay (10 ± 7 vs. 7 ± 4 days; P < 0.0001). The incidence of AKI increased in parallel with the extent of lung resection. Among the independent predictors of AKI, serum creatinine (area under the curve [AUC] 0.70 [95% CI 0.67-0.74]) and NT-proBNP (AUC 0.71 [95% CI 0.67-0.74]) provided the highest predictive accuracy, and their combination further significantly improved AKI prediction (AUC 0.74 [95% CI 0.71-0.77]). No difference in AKI prediction was observed between preoperative and postoperative NT-proBNP (P = 0.84). CONCLUSIONS: Acute kidney injury occurs in 10% of patients undergoing lung cancer surgery, and it is associated with a high incidence of postoperative complications. The risk of AKI can be accurately predicted by the combined evaluation of preoperative serum creatinine and NT-proBNP.

Acute Kidney Injury in Diabetic Patients With Acute Myocardial Infarction: Role of Acute and Chronic Glycemia.

BACKGROUND: In acute myocardial infarction, acute hyperglycemia is a predictor of acute kidney injury (AKI), particularly in patients without diabetes mellitus. This emphasizes the importance of an acute glycemic rise rather than glycemia level at admission. We investigated whether, in diabetic patients with acute myocardial infarction, the combined evaluation of acute and chronic glycemic levels may have better prognostic value for AKI than admission glycemia. METHODS AND RESULTS: At admission, we prospectively measured glycemia and estimated average chronic glucose levels (mg/dL) using glycosylated hemoglobin (HbA1c), according to the following formula: 28.7×HbA1c (%)-46.7. We evaluated the association with AKI of the acute/chronic glycemic ratio and of the difference between acute and chronic glycemia (ΔA-C). We enrolled 474 diabetic patients with acute myocardial infarction. Of them, 77 (16%) experienced AKI. The incidence of AKI increased in parallel with the acute/chronic glycemic ratio (12%, 14%, 22%; P=0.02 for trend) and ΔA-C (13%, 13%, 23%; P=0.01) but not with admission glycemic tertiles (P=0.22). At receiver operating characteristic analysis, the acute/chronic glycemic ratio (area under the curve: 0.62 [95% confidence interval, 0.55-0.69]; P=0.001) and ΔA-C (area under the curve: 0.62 [95% confidence interval, 0.54-0.69]; P=0.002) accurately predicted AKI, without difference in the area under the curve between them (P=0.53). At reclassification analysis, the addition of the acute/chronic glycemic ratio and ΔA-C to acute glycemia allowed proper AKI risk prediction in 16% of patients. CONCLUSIONS: In diabetic patients with acute myocardial infarction, AKI is better predicted by the combined evaluation of acute and chronic glycemic values than by assessment of admission glycemia alone.

Impact of Chronic Antiplatelet Therapy on Infarct Size and Bleeding in Patients With Acute Myocardial Infarction.

BACKGROUND: Patients hospitalized with acute myocardial infarction (AMI) are often on prior single antiplatelet therapy (SAPT) or a dual antiplatelet therapy (DAPT). Whether chronic SAPT or DAPT is beneficial or associated with an increased risk in AMI is still controversial. METHODS AND RESULTS: We prospectively enrolled 1718 consecutive patients with AMI (798 ST-segment elevation myocardial infarction and 920 non-ST-segment elevation myocardial infarction) who were divided according to their chronic APT (no APT, SAPT, or DAPT). The study primary end point was the infarct size, as estimated by troponin I peak. Incidence of major bleeding was also evaluated. Five hundred thirty-six (31%) patients were on chronic SAPT and 215 (13%) on DAPT. A graded increase in Global Registry of Acute Coronary Events (GRACE) and Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines (CRUSADE) risk scores was found going from patients without APT to those with DAPT, while a progressive smaller troponin I peak was observed with the increasing number of chronic antiplatelet agents (11.2 [interquartile range: 2-45] ng/mL, 6.6 [1-33] ng/mL, and 4.1 [1-24] ng/mL; P < .001 for trend). This result was maintained after adjustment for baseline ischemic risk profile (GRACE score) and other major confounders ( P < .001). The incidence of bleeding was higher in patients on chronic APT than in those without APT (5.2% vs 2.4%; P = .002). However, when the bleeding risk was adjusted for the CRUSADE risk score, chronic SAPT (odds ratio [OR]: 1.40, 95% confidence interval [CI]: 0.77-2.53) and DAPT (OR: 0.70, 95% CI: 0.29-1.70) were not associated with an increased bleeding risk. CONCLUSION: In patients with AMI, chronic APT is associated with higher baseline ischemic and bleeding risks. Despite this and unexpectedly, they have a smaller infarct size and similar adjusted bleeding risk.

Light sedation with dexmedetomidine: a practical approach for the intensivist in different ICU patients.

Light sedation, corresponding to a Richmond Agitation-Sedation Scale between 0 and -1 is a priority of modern critical care practice. Dexmedetomidine, a highly selective, central, α2-adrenoceptor agonist, is increasingly administered in the intensive care units (ICUs) as an effective drug to induce light sedation, analgesia and a quasi-physiological sleep in critically ill patients. Although in general dexmedetomidine is well tolerated, side effects as bradycardia, hypertension, and hypotension may occur. Although a general dosing range is suggested, different ICU patients may require different and highly precise titration that may significantly vary due to neurological status, cardio-respiratory function, base-line blood pressure, heart rate, liver efficiency, age and co-administration of other sedatives. This review analyzes the use of dexmedetomidine in different settings including pediatric, adult, medical and surgical patients starting with some considerations on delirium prevention and sleep quality in critically ill patients and how dexmedetomidine may contribute to these crucial aspects. Dexmedetomidine use in specific sub-populations with unique characteristics will be detailed, with a special attention to a safe use.

Prognostic Value of the Acute-to-Chronic Glycemic Ratio at Admission in Acute Myocardial Infarction: A Prospective Study.

OBJECTIVE: Acute hyperglycemia is a powerful predictor of poor prognosis in acute myocardial infarction (AMI), particularly in patients without diabetes. This emphasizes the importance of an acute glycemic rise rather than glycemia level at admission alone. We investigated in AMI whether the combined evaluation of acute and chronic glycemic levels, as compared with admission glycemia alone, may have a better prognostic value. RESEARCH DESIGN AND METHODS: We prospectively measured admission glycemia and estimated average chronic glucose levels (mg/dL) by the following formula: [(28.7 × glycosylated hemoglobin %) - 46.7], and calculated the acute-to-chronic (A/C) glycemic ratio in 1,553 consecutive AMI patients (mean ± SD age 67 ± 13 years). The primary end point was the combination of in-hospital mortality, acute pulmonary edema, and cardiogenic shock. RESULTS: The primary end point rate increased in parallel with A/C glycemic ratio tertiles (5%, 8%, and 20%, respectively; P for trend <0.0001). A parallel increase was observed in troponin I peak value (15 ± 34 ng/mL, 34 ± 66 ng/mL, and 68 ± 131 ng/mL; P < 0.0001). At multivariable analysis, A/C glycemic ratio remained an independent predictor of the primary end point and of troponin I peak value, even after adjustment for major confounders. At reclassification analyses, A/C glycemic ratio showed the best prognostic power in predicting the primary end point as compared with glycemia at admission in the entire population (net reclassification improvement 12% [95% CI 4-20]; P = 0.003) and, particularly, in patients with diabetes (27% [95% CI 14-40]; P < 0.0001). CONCLUSIONS: In AMI patients with diabetes, A/C glycemic ratio is a better predictor of in-hospital morbidity and mortality than glycemia at admission.

Renal replacement therapy in patients with acute myocardial infarction: Rate of use, clinical predictors and relationship with in-hospital mortality.

OBJECTIVES: We evaluated the rate of use, clinical predictors, and in-hospital outcome of renal replacement therapy (RRT) in acute myocardial infarction (AMI) patients. METHODS: All consecutive AMI patients admitted to the Coronary Care Unit between January 1st, 2005 and December 31st, 2015 were identified through a search of our prospectively collected clinical database. Patients were grouped according to whether they required RRT or not. RESULTS: Two-thousand-eight-hundred-thirty-nine AMI patients were included. Eighty-three (3%) AMI patients underwent RRT. Variables confirmed at cross validation analysis to be associated with RRT were: admission creatinine >1.5mg/dl (OR 16.9, 95% CI 10.4-27.3), cardiogenic shock (OR 23.0, 95% CI 14.4-36.8), atrial fibrillation (OR 8.6, 95% CI 5.5-13.4), mechanical ventilation (OR 22.6, 95% CI 14.2-36.0), diabetes mellitus (OR 4.8, 95% CI 3.1-7.4), and left ventricular ejection fraction <40% (OR 9.1, 95% CI 5.6-14.7). The AUC for RRT with the combination of these predictors was 0.96 (95% CI 0.94-0.97; P<0.001). In-hospital mortality was significantly higher in RRT patients (41% vs. 2.1%, P<0.001). Oligoanuria as indication for RRT (OR 5.1, 95% CI 1.7-15.4), atrial fibrillation (OR 4.3, 95% CI 1.6-11.5), mechanical ventilation (OR 20.8, 95% CI 6.1-70.4), and cardiogenic shock (OR 12.9, 95% CI 4.4-38.3) independently predicted mortality in RRT-treated patients. The AUC for in-hospital mortality prediction with the combination of these variables was 0.92 (95% CI 0.87-0.98; P<0.001). CONCLUSIONS: Patients with AMI undergoing RRT had strikingly high in-hospital mortality. Use of RRT and its associated mortality were accurately predicted by easily obtainable clinical variables.