Development of a severe mesenteric traction syndrome during major abdominal surgery is associated with increased postoperative morbidity: Secondary data analysis on prospective cohorts.

PURPOSE: MTS is elicited during open abdominal surgery and is characterized by facial flushing, hypotension, and tachycardia in response to the release of prostacyclin (PGI2) to plasma. MTS seems to affect postoperative morbidity, but data from larger cohorts are lacking. We aimed to determine the impact of severe mesenteric traction syndrome (MTS) on postoperative morbidity in patients undergoing open upper gastrointestinal surgery. METHODS: The study was a secondary analysis of data from three cohorts (n = 137). The patients were graded for severity of MTS intraoperatively, and hemodynamic variables and blood samples for plasma 6-keto-PGF1α, a stable metabolite of PGI2, were obtained at defined time points. Postoperative morbidity was evaluated by the comprehensive complication index (CCI) and the Dindo-Clavien classification (DC). RESULTS: Patients undergoing either esophagectomy (n = 70), gastrectomy (n = 22), liver- (n = 23), or pancreatic resection (n = 22) were included. Severe MTS was significantly associated with increased postoperative morbidity, i.e., CCI ≥ 26.2 (OR 3.06 [95% CI 1.1-6.6]; p = 0.03) and risk of severe complications, i.e., DC ≥3b (OR 3.1 [95% CI 1.2-8.2]; p = 0.023). Furthermore, patients with severe MTS had increased length of stay (OR 10.1 [95% CI 1.9-54.3]; p = 0.007) and were more likely to be admitted to the intensive care unit (OR = 7.3 [95% CI 1.3-41.9]; p = 0.027), but there was no difference in 1-year mortality. CONCLUSION: Occurrence of severe MTS during upper gastrointestinal surgery is associated with increased postoperative morbidity as indicated by an increased rate of severe complications, length of stay, and admission to the ICU. It remains to be determined whether inhibition of MTS enhances postoperative recovery.

Combined Analysis of Human and Experimental Murine Samples Identified Novel Circulating MicroRNAs as Biomarkers for Atrial Fibrillation.

BACKGROUND: Recent experimental studies have demonstrated that several microRNAs (miRNAs) expressed in atrial tissue promote a substrate of atrial fibrillation (AF). However, because it has not been fully elucidated whether these experimental data contribute to identifying circulating miRNAs as biomarkers for AF, we used a combined analysis of human serum and murine atrial samples with the aim of identifying these biomarkers for predicting AF.Methods and Results:Comprehensive analyses were performed to screen 733 miRNAs in serum from 10 AF patients and 5 controls, and 672 miRNAs in atrial tissue from 6 inducible atrial tachycardia model mice and 3 controls. We selected miRNAs for which expression was detected in both analyses, and their expression levels were changed in the human analyses, the murine analyses, or both. This screening identified 11 candidate miRNAs. Next, we quantified the selected miRNAs using a quantitative RT-PCR in 50 AF and 50 non-AF subjects. The individual assessment revealed that 4 miRNAs (miR-99a-5p, miR-192-5p, miR-214-3p, and miR-342-5p) were significantly upregulated in AF patients. A receiver-operating characteristics curve indicated that miR-214-3p and miR-342-5p had the highest accuracy. The combination of the 4 miRNAs modestly improved the predictive accuracy for AF (76% sensitivity, 80% specificity). CONCLUSIONS: Novel circulating miRNAs were upregulated in the serum of AF patients and might be potential biomarkers of AF.

Comparison of risk assessment strategies for not-high-risk pulmonary embolism.

We compared the prognostic performance of the 2014 European Society of Cardiology (ESC) risk stratification algorithm with the previous 2008 ESC algorithm, the Bova score and the modified FAST score (based on a positive heart-type fatty acid-binding protein (H-FABP) test, syncope and tachycardia, modified using high-sensitivity troponin T instead of H-FABP) in 388 normotensive pulmonary embolism patients included in a single-centre cohort study.Overall, 25 patients (6.4%) had an adverse 30-day outcome. Regardless of the score or algorithm used, the rate of an adverse outcome was highest in the intermediate-high-risk classes, while all patients classified as low-risk had a favourable outcome (no pulmonary embolism-related deaths, 0-1.4% adverse outcome). The area under the curve for predicting an adverse outcome was higher for the 2014 ESC algorithm (0.76, 95% CI 0.68-0.84) compared with the 2008 ESC algorithm (0.65, 95% CI 0.56-0.73) and highest for the modified FAST score (0.82, 95% CI 0.75-0.89). Patients classified as intermediate-high-risk by the 2014 ESC algorithm had a 8.9-fold increased risk for an adverse outcome (3.2-24.2, p<0.001 compared with intermediate-low- and low-risk patients), while the highest OR was observed for a modified FAST score ≥3 points (OR 15.9, 95% CI 5.3-47.6, p<0.001).The 2014 ESC algorithm improves risk stratification of not-high-risk pulmonary embolism compared with the 2008 ESC algorithm. All scores and algorithms accurately identified low-risk patients, while the modified FAST score appears more suitable to identify intermediate-high-risk patients.

High-fat diet and chronic stress reduce central pressor and tachycardic effects of apelin in Sprague-Dawley rats.

Central application of apelin elevates blood pressure and influences neuroendocrine responses to stress and food consumption. However, it is not known whether the central cardiovascular effects of apelin depend also on caloric intake or chronic stress. The purpose of the present study was to determine the effects of intracerebroventricular administration of apelin on blood pressure (mean arterial blood pressure) and heart rate in conscious Sprague-Dawley rats consuming either a normal-fat diet (NFD) or high-fat diet (HFD) for 12 weeks. During the last 4 weeks of the food regime, the rats were exposed (NFDS and HFDS groups) or not exposed (NFDNS and HFDNS groups) to chronic stress. Each group was divided into two subgroups receiving intracerebroventricular infusions of either vehicle or apelin. Apelin elicited significant increase of mean arterial blood pressure and heart rate in the NFDNS rats. This effect was abolished in the HFDNS, HFDS and NFDS groups. HFD resulted in a significant elevation of blood concentrations of total cholesterol, triglycerides glucose and insulin. Chronic stress reduced plasma concentration of total and high-density lipoprotein cholesterol, and increased plasma corticosterone concentration and APJ receptor mRNA expression in the hypothalamus, whereas a combination of a HFD with chronic stress resulted in the elevation of plasma triglycerides, total cholesterol and low-density lipoprotein cholesterol, and in increased plasma corticosterone concentration, apelin concentration and APJ receptor mRNA expression in the hypothalamus. It is concluded that a HFD and chronic stress result in significant suppression of the central pressor action of apelin, and cause significant though not unidirectional changes of metabolic and endocrine parameters.

Clinical outcomes of ED patients with bandemia.

BACKGROUND: Although an elevated white blood cell count is a widely utilized measure for evidence of infection and an important criterion for evaluation of systemic inflammatory response syndrome, its component band count occupies a more contested position within clinical emergency medicine. Recent studies indicate that bandemia is highly predictive of a serious infection, suggesting that clinicians who do not appreciate the value of band counts may delay diagnosis or overlook severe infections. OBJECTIVES: Whereas previous studies focused on determining the quantitative value of the band count (ie, determining sensitivity, threshold for bandemia, etc.), this study directs attention to patient-centered outcomes, hypothesizing that the degree of bandemia predisposes patients to subsequent negative clinical outcomes associated with underappreciated severe infections. METHODS: This retrospective study of electronic medical records includes patients who initially presented to the emergency department (ED) with bandemia and were subsequently discharged from the ED. These patients were screened for repeat ED visits within 7 days and death within 30 days. RESULTS: In patients with severe bandemia who were discharged from the ED, there was a 20.9% revisit rate at 7 days and a 4.9% mortality rate at 30 days, placing severely bandemic patients at 5 times significantly greater mortality compared to nonbandemic patients (P = .032). CONCLUSION: Our review of patient outcomes suggests that the degree of bandemia, especially in the setting of concurrent tachycardia or fever, is associated with greater likelihood of negative clinical outcomes.

Vascular Dilation, Tachycardia, and Increased Inotropy Occur Sequentially with Increasing Epinephrine Dose Rate, Plasma and Myocardial Concentrations, and cAMP.

BACKGROUND: While epinephrine infusion is widely used in critical care for inotropic support, there is no direct method to detect the onset and measure the magnitude of this response. We hypothesised that surrogate measurements, such as heart rate and vascular tone, may indicate if the plasma and tissue concentrations of epinephrine and cAMP are in a range sufficient to increase myocardial contractility. METHODS: Cardiovascular responses to epinephrine infusion (0.05-0.5 mcgkg(-1)min(-1)) were measured in rats using arterial and left ventricular catheters. Epinephrine and cAMP levels were measured using ELISA techniques. RESULTS: The lowest dose of epinephrine infusion (0.05 mcgkg(-1)min(-1)) did not raise plasma epinephrine levels and did not lead to cardiovascular response. Incremental increase in epinephrine infusion (0.1 mcgkg(-1)min(-1)) elevated plasma but not myocardial epinephrine levels, providing vascular, but not cardiac effects. Further increase in the infusion rate (0.2 mcgkg(-1)min(-1)) raised myocardial tissue epinephrine levels sufficient to increase heart rate but not contractility. Inotropic and lusitropic effects were significant at the infusion rate of 0.3 mcgkg(-1)min(-1). Correlation of plasma epinephrine to haemodynamic parameters suggest that as plasma concentration increases, systemic vascular resistance falls (EC50=47 pg/ml), then HR increases (ED50=168 pg/ml), followed by a rise in contractility and lusitropy (ED50=346 pg/ml and ED50=324 pg/ml accordingly). CONCLUSIONS: The dose response of epinephrine is distinct for vascular tone, HR and contractility. The need for higher doses to see cardiac effects is likely due to the threshold for drug accumulation in tissue. Successful inotropic support with epinephrine cannot be achieved unless the infusion is sufficient to raise the heart rate.

Two-week normobaric intermittent hypoxia exposures enhance oxyhemoglobin equilibrium and cardiac responses during hypoxemia.

Intermittent hypoxia (IH) is extensively applied to challenge cardiovascular and respiratory function, and to induce physiological acclimatization. The purpose of this study was to test the hypothesis that oxyhemoglobin equilibrium and tachycardiac responses during hypoxemia were enhanced after 14-day IH exposures. Normobaric-poikilocapnic hypoxia was induced with inhalation of 10% O2 for 5-6 min interspersed with 4 min recovery on eight nonsmokers. Heart rate (HR), arterial O2 saturation (SaO 2), and end-tidal O2 (PetO 2) were continuously monitored during cyclic normoxia and hypoxia. These variables were compared during the first and fifth hypoxic bouts between day 1 and day 14. There was a rightward shift in the oxyhemoglobin equilibrium response following 14-day IH exposures, as indicated by the greater PetO 2 (an index of arterial Po2) at 50% of SaO 2 on day 14 compared with day 1 [33.9 ± 1.5 vs. 28.2 ± 1.3 mmHg (P = 0.005) during the first hypoxic bout and 39.4 ± 2.4 vs. 31.4 ± 1.5 mmHg (P = 0.006) during the fifth hypoxic bout] and by the augmented gains of ΔSaO 2/ΔPetO 2 (i.e., deoxygenation) during PetO 2 from 65 to 40 mmHg in the first (1.12 ± 0.08 vs. 0.80 ± 0.02%/mmHg, P = 0.001) and the fifth (1.76 ± 0.31 vs. 1.05 ± 0.06%/mmHg, P = 0.024) hypoxic bouts. Repetitive IH exposures attenuated (P = 0.049) the tachycardiac response to hypoxia while significantly enhancing normoxic R-R interval variability in low-frequency and high-frequency spectra without changes in arterial blood pressure at rest or during hypoxia. We conclude that 14-day IH exposures enhance arterial O2 delivery and improve vagal control of HR during hypoxic hypoxemia.

Cyclic vomiting associated with excessive dopamine in Riley-day syndrome.

GOALS: To analyze the neurochemical profile during the recurrent attacks of nausea and vomiting in patients with Riley-day syndrome. BACKGROUND: One of the most disabling features of patients with Riley-day syndrome are recurrent attacks of severe nausea/retching/vomiting accompanied by hypertension, tachycardia, and skin flushing, usually triggered by emotional or other stresses. STUDY: We monitored blood pressure and heart rate and measured plasma catecholamines during typical dysautonomic crises triggered by emotionally charged situations. For comparison, measurements were repeated at follow-up after the symptoms had resolved and the patients were feeling calm and well. RESULTS: During a typical attack, patients were hypertensive and tachycardic. In all patients, circulating levels of norepinephrine (P < 0.002) and dopamine (P < 0.007) increased significantly. CONCLUSIONS: Activation of dopamine receptors in the chemoreceptor trigger zone may explain the cyclic nausea/retching/vomiting of patients with Riley-day syndrome.

Diastolic hypotension is an unrecognized risk factor for ß-agonist-associated myocardial injury in children with asthma.

OBJECTIVES: Tachycardia and diastolic hypotension have been associated with ß-2 agonist use. In the setting of ß-agonist-induced chronotropy and inotropy, diastolic hypotension may limit myocardial blood flow. We hypothesized that diastolic hypotension is associated with ß-agonist use and that diastolic hypotension and tachycardia are associated with biochemical evidence of myocardial injury in children with asthma. DESIGN: Two patient cohorts were collected. The first, consisting of patients transported for respiratory distress having received at least 10 mg of albuterol, was studied for development of tachycardia and hypotension. The second, consisting of patients who had troponin measured during treatment for status asthmaticus with continuous albuterol, was studied for factors associated with elevated troponin. Exclusion criteria for both cohorts included age younger than 2 years old, sepsis, pneumothorax, cardiac disease, and antihypertensive use. Albuterol dose, other medications, and vital signs were collected. Diastolic and systolic hypotension were defined as an average value below the fifth percentile for age and tachycardia as average heart rate above the 98th percentile for age. PATIENTS: Ninety of 1,390 children transported for respiratory distress and 64 of 767 children with status asthmaticus met inclusion criteria. MEASUREMENTS AND MAIN RESULTS: Diastolic hypotension occurred in 56% and 98% of the first and second cohorts, respectively; tachycardia occurred in 94% and 95% of the first and second cohorts, respectively. Diastolic hypotension and tachycardia had a weak linear correlation with albuterol dose (p = 0.02 and p = 0.005, respectively). Thirty-six percent had troponin > 0.1 ng/mL (range, 0-12.6). In multivariate analysis, interaction between diastolic hypotension and tachycardia alone was associated with elevated troponin (p = 0.02). CONCLUSIONS: Diastolic hypotension and tachycardia are dose-dependent side effects of high-dose albuterol. In high-risk patients with status asthmaticus treated with albuterol, diastolic hypotension and tachycardia are associated with biochemical evidence of myocardial injury. Diastolic hypotension, especially combined with tachycardia, could be a reversible risk factor for myocardial injury related to ß-agonist use.

Uridine treatment prevents myocardial injury in rat models of acute ischemia and ischemia/reperfusion by activating the mitochondrial ATP-dependent potassium channel.

The effect of uridine on the myocardial ischemic and reperfusion injury was investigated. A possible mechanism of its cardioprotective action was established. Two rat models were used: (1) acute myocardial ischemia induced by occlusion of the left coronary artery for 60 min; and (2) myocardial ischemia/reperfusion with 30-min ischemia and 120-min reperfusion. In both models, treatment with uridine (30 mg/kg) prevented a decrease in cell energy supply and in the activity of the antioxidant system, as well as an increase in the level of lipid hydroperoxides and diene conjugates. This led to a reduction of the necrosis zone in the myocardium and disturbances in the heart rhythm. The blocker of the mitochondrial ATP-dependent potassium (mitoKATP) channel 5-hydroxydecanoate limited the positive effects of uridine. The data indicate that the cardioprotective action of uridine may be related to the activation of the mitoKATP channel. Intravenously injected uridine was more rapidly eliminated from the blood in hypoxia than in normoxia, and the level of the mitoKATP channel activator UDP in the myocardium after uridine administration increased. The results suggest that the use of uridine can be a potentially effective approach to the management of cardiovascular diseases.

A pre-existent elevated C-reactive protein is associated with the recurrence of atrial tachyarrhythmias after catheter ablation in patients with atrial fibrillation.

AIMS: It has been reported that an inflammatory process is involved in the development of atrial fibrillation (AF). In this study, we examined the hypothesis that a pre-existent inflammatory response may enhance the recurrence of AF after catheter ablation (CA). METHODS AND RESULTS: A total of 257 consecutive AF patients undergoing CA were enrolled in this study. The C-reactive protein was assessed by a high-sensitive radio-immunoassay 1 day before the procedure. Of the clinical characteristics, an advanced age, structural heart disease, and the left atrial (LA) diameter were significantly increased when the C-reactive protein level was elevated. Atrial fibrillation occurrences were significantly increased when the C-reactive protein level was elevated. A multivariate analysis demonstrated that an elevated C-reactive protein level [hazard ratio (95% CI); 2.23 (1.04-4.35)], the LA diameter [1.26 (1.10-1.66)], and persistent AF duration [2.13 (1.13-3.79)] were independent factors related to the recurrence of AF after CA. In the procedural findings, burst-inducible AF after pulmonary vein (PV) isolation was significantly increased, and the incidence of AF from the PVs was significantly lower when the C-reactive protein level was elevated. CONCLUSION: An elevated C-reactive protein level was associated with atrial structural and electrical remodelling maintaining AF, and the increased re-entrant atrial substrate might increase the recurrence of AF after the CA procedure.

[Severe circulatory insufficiency in a patient with neonatal hyperthyroidism]. / Súlyos keringési elégtelenséggel járó neonatalis hyperthyreosis.

Authors describe a case of a premature infant whose mother had a history of thyroidectomy due to Graves' disease and her hormonal status was not controlled during pregnancy. She did not receive prenatal care and on 33rd week the premature infant was delivered by emergency cesarean section because of fetal tachycardia and imminent intrauterine asphyxia. The infant with a weight of 1350 gram (percentile <10) was dysmature and had a large struma. The newborn received both conventional and high frequency ventilation for respiratory insufficiency and was treated with beta-blocker, digoxin and dobutamine for severe tachycardia (>180/min) and cardiac decompensation. Further examinations proved cardiomegaly, pericardial fluid, severe pulmonary hypoplasia, mitral- and tricuspid insufficiency and hepatosplenomegaly. The level of free thyroid hormones was several times higher than normal (fT4: > 6 ng/dl, fT3 > 30 pg/ml), while TSH level was 0. Respiratory support was required for 7 days, inotropic support for 10 days; at the same time propranolol and K-iodide were administered. Eventually, the tachycardia settled and beta-blocker therapy was continued with reduced doses. Finally, the thyroid hormone levels became normal. Authors emphasize that newborns of women suffering from Graves' disease can significantly lag behind in weight increase, may have severe circulatory insufficiency and symptoms of thyrotoxicosis. We also emphasize the importance of the monitoring maternal hormone levels and antibody titers.

Case of multisystem inflammatory syndrome in children presenting as fever and abdominal pain.

This case aims to remind all providers to scrutinise for atypical presentations of multisystem inflammatory syndrome in children (MIS-C) which may mimic a more routine diagnosis. In the absence of mucocutaneous symptoms, the diagnosis of MIS-C can be missed. Given the potential for rapid deterioration of patients with MIS-C, early treatment and inpatient interventions are necessary.

Heart rate reduction by ivabradine reduces oxidative stress, improves endothelial function, and prevents atherosclerosis in apolipoprotein E-deficient mice.

BACKGROUND: Elevated heart rate is associated with increased cardiovascular morbidity. We hypothesized that selective heart rate reduction may influence endothelial function and atherogenesis and tested the effects of the I(f) current inhibitor ivabradine in apolipoprotein E-deficient mice. METHODS AND RESULTS: Male apolipoprotein E-deficient mice fed a high-cholesterol diet were treated with ivabradine (10 mg . kg(-1) . d(-1)) or vehicle for 6 weeks (n=10 per group). Ivabradine reduced heart rate by 13.4% (472+/-9 versus 545+/-11 bpm; P<0.01) but did not alter blood pressure or lipid levels. Endothelium-dependent relaxation of aortic rings was significantly improved in ivabradine-fed animals (P<0.01). Ivabradine decreased atherosclerotic plaque size in the aortic root by >40% and in the ascending aorta by >70% (P<0.05). Heart rate reduction by ivabradine had no effect on the number of endothelial progenitor cells and did not alter aortic endothelial nitric oxide synthase, phosphorylated Akt, vascular cell adhesion molecule-1, or intercellular adhesion molecule-1 expression but decreased monocyte chemotactic protein-1 mRNA and exerted potent antioxidative effects. Ivabradine reduced vascular NADPH oxidase activity to 48+/-6% and decreased markers of superoxide production and lipid peroxidation in the aortic wall (P<0.05). The in vivo effects of ivabradine were absent at a dose that did not lower heart rate, in aortic rings treated ex vivo, and in cultured vascular cells. In contrast to ivabradine, treatment with hydralazine (25 mg . kg(-1) . d(-1) for 6 weeks) reduced blood pressure (-15%) but increased heart rate (37%) and did not improve endothelial function, atherosclerosis, or oxidative stress. CONCLUSIONS: Selective heart rate reduction with ivabradine decreases markers of vascular oxidative stress, improves endothelial function, and reduces atherosclerotic plaque formation in apolipoprotein E-deficient mice.

D-Dimer Predicts Disease Severity but Not Long-Term Prognosis in Acute Pulmonary Embolism.

D-dimer might be correlated with prognosis in pulmonary embolism (PE). The predictive value of plasma D-dimer for disease severity and survival was investigated in the lowest and highest D-dimer quartile among 200 patients with PE. Patients with high D-dimers were significantly more often hypotensive (P = .001), tachycardic (P = .016), or hypoxemic (P = .001). Pulmonary arterial obstruction index (PAOI) values were significantly higher in the high D-dimer quartile (P < .001). Elevated troponin I (TNI) levels (P < .001), simplified PE severity indices ≥1 (P < .001), right-to-left ventricular (RV/LV) diameter ratios ≥1 (P < .001), and thrombolysis (P = .001) were more frequent in the high D-dimer quartile. D-dimer was associated with RV/LV ratios ≥1 (P = .021), elevated PAOI (P < .001) or TNI levels (P < .001), hypotension (P < .001), tachycardia (P = .003), and hypoxemia (P < .001), but not with long-term all-cause mortality. D-dimer predicts disease severity but not long-term prognosis in acute PE, possibly due to a more aggressive treatment strategy in severely affected patients.

Time- and dose-related regional fluxes of tissue-type plasminogen activator in anesthetized endotoxemic pigs.

BACKGROUND: Acute endotoxinemia elicits an early fibrinolytic response. This study analyzes the effects of the dose and duration of endotoxin infusion on arterial levels of tissue-type plasminogen activator (tPA) and pulmonary, mesenteric and hepatic plasma tPA fluxes. METHODS: Pigs were randomized to receive an acute, high-dose (for 6 h, n=13, high ETX) or a prolonged, low-dose (for 18 h, n=18, low ETX) infusion of endotoxin or saline vehicle alone (for 18 h, n=14, control). All animals were fluid resuscitated to maintain a normodynamic circulation. Systemic and regional blood flows were measured and arterial, pulmonary arterial, portal and hepatic venous blood samples were analyzed to calculate regional net fluxes of tPA. Plasma tumor necrosis factor (TNF-alpha) levels were analyzed. RESULTS: Mesenteric tPA release and hepatic uptake increased maximally at 1.5 h in ETX groups related to dose. Maximal mesenteric tPA release [high ETX 612 (138-1185) microg/min/kg, low ETX 72 (32-94) microg/min/kg, median+/-interquartile range] and hepatic tPA uptake [high ETX -1549 (-1134 to -2194) microg/min/kg, low ETX -153 (-105 to -307) microg/min/kg] correlated to TNF-alpha levels. Regional tPA fluxes returned to baseline levels at 6 h in both ETX groups and also remained low during sustained low ETX. No changes were observed in control animals. CONCLUSIONS: Endotoxemia induces an early increase in mesenteric tPA release and hepatic tPA uptake related to the severity of endotoxemia. The time patterns of changes in mesenteric and hepatic tPA fluxes are similar in acute high-dose endotoxemia and sustained low-dose endotoxemia.

Lower In-Hospital Ventricular Tachyarrhythmia in Patients With Acute Myocardial Infarction Receiving Prior Statin Therapy.

We evaluated whether prior statin therapy reduces in-hospital ventricular tachycardia/ventricular fibrillation (VT/VF) in percutaneous coronary intervention (PCI) patients with acute myocardial infarction (MI). Among the 1177 patients from the Acute Myocardial Infarction Registry-National Institutes of Health (KAMIR-NIH), 823 (70%) patients received prior statin therapy. Prior statin therapy was associated with a reduced risk of VT/VF events in both adjusted propensity score analysis (odds ratio [OR] 0.414, 95% confidence interval [CI], 0.198-0.865, P = .019) and adjusted inverse probability of treatment weight analysis (OR 0.463, 95% CI, 0.216-0.994, P = .048). The risk of in-hospital death did not differ significantly between those with or without prior statin therapy (hazard ratio [HR] 0.416, 95% CI, 0.112-1.548, P = .191). Major adverse cardiac events occurred in 116 (8.9%) patients during follow-up. Prior statin therapy was associated with a lower risk of major adverse cardiac events during the follow-up period (HR 0.486, 95% CI, 0.243-0.974, P = .042); however, this was mainly driven by reduced noncardiac death. Prior statin therapy might reduce the incidence of serious cardiac tachyarrhythmia, such as VT/VF, in patients with MI undergoing PCI. However, the reduction in VT/VF due to prior statin therapy did not improve short- and long-term clinical outcomes.

High sensitivity troponin in the management of tachyarrhythmias.

BACKGROUND: The introduction of the highly sensitive troponin (hs-trop) assays into clinical practice has allowed for the more rapid diagnosis or exclusion of type 1 myocardial infarctions (T1MI) by clinicians, in addition type 2 myocardial infarctions (T2MI) are now more frequently detected. Tachyarrhythmias are one of the common causes of T2MI, the medium and long term outcome for this cohort of T2MI is yet to be clarified. METHODS: Retrospective review of consecutive patients admitted with a diagnosis of either (a) non ST-elevation myocardial infarction (NSTEMI) or (b) tachyarrhythmia was performed. Data were collected on patient demographics and investigations. Patient mortality status was recorded through the Personal Demographics Service (PDS) via NHS Digital. RESULTS: A total of 704 patients were eligible for inclusion to the study. 264 patients were included in the study with a final discharge diagnosis of NSTEMI and 440 patients with a final discharge diagnosis of tachyarrhythmia. There was a significantly higher peak troponin in NSTEMI patients compared to the tachyarrhythmia troponin positive group (4552ng/L vs 571ng/L, p<0.001). Mortality was significantly higher in the troponin positive tachyarrhythmia patients than the troponin negative patients (54 vs 34, 26.2% vs 14.5%, log rank p=0.003), furthermore, the mortality of NSTEMI and troponin positive tachyarrhythmia patients was similar (55 vs 54, 20.8% vs 26.2%, log rank p=0.416). Only one patient (0.14%) was given a formal diagnosis of T2MI. CONCLUSIONS: These data suggest that troponin positive tachyarrhythmia is not a benign diagnosis, and has a mortality rate similar to NSTEMI. Formal labeling as T2MI is rare in real life practice. More investigation into the detection and management of T2MI and troponin positive arrhythmia patients is now warranted.