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Background The prognostic role of diabetes mellitus (DM) in heart failure (HF) patients is undefined, since DM is outweighed by several DM-related variables when confounders are considered. We determined the prognostic role of DM, treatment, and glycemic control in a real-life HF population. Methods 3927 HF patients included in the Metabolic Exercise Cardiac Kidney Index (MECKI) score database were evaluated with a median follow-up of 3.66 years (IQR 1.70–6.67). Data analysis considered survival between DM (n = 897) vs. non-DM (n = 3030) patients, and, in diabetics, between insulin (n = 304), oral antidiabetics (n = 479), and dietary only (n = 88) treatments. The role of glycemic control was evaluated grouping DM patients according to glycated hemoglobin (HbA1c): 8% (n = 149). All analyses were performed also adjusting for ejection fraction, renal function, hemoglobin, sodium, exercise peak oxygen uptake, and ventilation/carbon dioxide relationship slope. Study primary endpoint was the composite of cardiovascular death, urgent heart transplantation, or left ventricular assist device implantation. Secondary endpoints were cardiovascular and all causes death. Results For all endpoints, upon adjustment for confounders, DM status and insulin treatment or dietary regimen were not significantly associated with adverse long-term prognosis compared to non-DM and oral antidiabetic treated patients, respectively. A worse prognosis was observed in HbA1c >8% patients (Log-Rank p Conclusion In HF patients, DM, insulin treatment and dietary regimen are not adverse outcome predictors. The only condition related to long-term prognosis, considering potential confounders, is poor glycemic control.

The usefulness of β-blockers in heart failure (HF) patients with permanent atrial fibrillation (AF) has been questioned. Background: The usefulness of β-blockers in heart failure (HF) patients with permanent atrial fibrillation (AF) has been questioned. Methods and results: We analyzed data from HF patients (958 patients (801 males, 84%, age 67 ± 11 years)) with AF enrolled in the MECKI score database. We evaluated prognosis (composite of cardiovascular death, urgent heart transplant, or left ventricular assist device) of patients receiving β-blockers (n = 777, 81%) vs. those not treated with β-blockers (n = 181, 19%). We also analyzed the role β1-selectivity and the role of daily β-blocker dose. To account for different HF severity, Kaplan-Meier survival curves were normalized for relevant confounding factors and for treatment strategies. Dose was available in 629 patients. Median follow-up was 1312 (577–2304) days in the entire population, 1203 (614–2420) and 1325 (569–2300) days in patients not receiving and receiving β-blockers. 224 (23%, 54/1000 events/year), 163 (21%, 79/1000 events/year), and 61 (34%, 49/1000 events/year) events were recorded, respectively. At 10-year patients treated with β-blockers had a better outcome (HR 0.447, p < 0.01) with no effects as regards β1selective drugs (53%) vs. β1-β2 blockers (47%). Survival improved in parallel with β-blocker dose increase (HR 0.296, 0.496, 0.490 for the high, medium, and low dose vs. no β-blockers, p < 0.0001). Conclusion: HF patients with AF taking a β-blocker have a better outcome (with a survival improvement in parallel with daily dose but no differences as regards β1 selectivity) but this does not mean that β-blockers improve outcomes in these patients as we cannot control for all the potential confounders associated with β-blocker use.

A shorter time to treatment has been shown to be associated with lower mortality rates in acute myocardial infarction (AMI). Several strategies have been adopted with the aim to reduce any delay in diagnosis of AMI: pre-hospital triage with telemedicine is one of such strategies. We therefore aimed to measure the real effect of pre-hospital triage with telemedicine in case of AMI in a meta-analysis study.We performed a meta-analysis of non-randomized studies with the aim to quantify the exact reduction of time to treatment achieved by pre-hospital triage with telemedicine. Data were pooled and compared by relative time reduction and 95% C.I.s. A meta-regression analysis was performed in order to find possible predictors of shorter time to treatment.Eleven studies were selected and finally evaluated in the study. The overall relative reduction of time to treatment with pre-hospital triage and telemedicine was -38/-40% (p0.001). Absolute time reduction was significantly correlated to time to treatment in the control groups (p0.001), while relative time reduction was independent. A non-significant trend toward shorter relative time reductions was observed over years.Pre-hospital triage with telemedicine is associated with a near halved time to treatment in AMI. The benefit is larger in terms of absolute time to treatment reduction in populations with larger delays to treatment.

The link between physical activity and the risk of atrial fibrillation (AF) remains controversial. We therefore sought to further assess by a meta-analysis whether increased levels of physical activity may increase the risk of AF. In October 2015, a PubMed research was conducted for studies that investigated this topic. We identified 11 relevant studies with a total of 81,787 participants. The pooled analysis did not show an increased risk of AF in subjects practicing physical activity (odds ratio (OR)=0.92, 95% C.I.=0.84-1.01, p=0.077, I(2)=90%). However, given the observed large heterogeneity among studies, a subgroup analysis was performed in order to identify possible variables influencing the risk of AF. Significantly higher risk of AF in subjects with reported physical activity was found in studies enrolling exclusively male participants (OR=7.49, 95% C.I.=3.12-19.01, p

Mortality following an admission for acute decompensated heart failure (ADHF) is high and risk stratification in this context remains a challenge. The objective of the present study was to assess whether a simple echocardiographic assessment of pulmonary hypertension (PH) and/or of right ventricular (RV) dysfunction is associated with cardiovascular events in a 1-year follow-up after hospital discharge.The present prospective longitudinal study included 214 patients admitted to hospital with a cardiologist-adjudicated diagnosis of ADHF and a left ventricular ejection fraction (LVEF) at echocardiography 40%. Echocardiography was performed at admission and at discharge and included pulmonary artery systolic pressure (PASP) and RV function as defined by the tricuspid annular plane systolic displacement (TAPSE). The primary end-point was the combination of all-cause mortality and re-hospitalization for worsening heart failure at 1 year after hospital discharge. During an average follow-up period of 230 ± 130 days, 40 patients died and 41 patients underwent re-hospitalization due to ADHF. At multivariate analysis the independent predictors were LVEF, PASP at discharge and creatinine plasma levels (all p 0.001). At ROC analysis the best threshold of PASP to discriminate low-risk from high-risk patients was 40 mm Hg.In ADHF patients with reduced LVEF, PH at discharge is a pivotal prognostic feature to predict morbidity/mortality within the first year after the acute episode.

Background In a recent paper Singh et al. analyzed the effect of drug treatment on recurrence of takotsubo cardiomyopathy (TTC) in a comprehensive meta-analysis. The study found that recurrence rates were independent of clinic utilization of BB prescription, but inversely correlated with ACEi/ARB prescription: authors therefore conclude that ACEi/ARB rather than BB may reduce risk of recurrence. Methods We aimed to re-analyze data reported in the study, now weighted for populations' size, in a meta-regression analysis. Results After multiple meta-regression analysis, we found a significant regression between rates of prescription of ACEi and rates of recurrence of TTC; regression was not statistically significant for BBs. Conclusions On the bases of our re-analysis, we confirm that rates of recurrence of TTC are lower in populations of patients with higher rates of treatment with ACEi/ARB. That could not necessarily imply that ACEi may prevent recurrence of TTC, but barely that, for example, rates of recurrence are lower in cohorts more compliant with therapy or more prescribed with ACEi because more carefully followed. Randomized prospective studies are surely warranted.

Background Prior meta-analysis studies showed that direct oral anticoagulants (DOAs) are as effective and safe as warfarin for the prevention of recurrences in patients with venous thrombo-embolism(VTE) and cancer. However, randomized studies also showed that low-molecular-weight-heparin (LMWH) performs better than warfarin in subjects with cancer. We therefore aimed to assess whether, even after pooling data with warfarin and LMWH, the use of DOAs remains safe and effective. Methods We performed a meta-analysis of randomized controlled trials with the aim of assessing the efficacy and safety of DOAs in patients with VTE and cancer. Data on recurrent VTE and major and clinically relevant nonmajor bleeding were analyzed. Data were pooled and compared by ORs and 95% CIs. Results Nine studies were included in the meta-analysis, seven in comparison with VKI, 2 with LMWH, accounting for a total of 1952 patients. VTE recurred in 5.4% and in 5.9% of patients with cancer treated with DOAs and conventional treatment, respectively (OR 0.79; 95% CI, 0.53–1.17; I 2 0%). Bleeding occurred in 10.8% and 11% of patients receiving DOAs and conventional treatment, respectively (OR 0.96; 95% CI, 0.71–1.30; I 2 , 44%). Higher bleeding rates were found when DOAs are compared with LMWH (OR 2.72, 95% CI, 1.05–7.01). Conclusions DOAs seem to be as effective and safe as conventional treatment for the prevention of VTE in patients with cancer in comparison with VKI. Higher bleeding rates were found when DOAs are compared with LMWH.

We report the case of an 81-year-old man who presented with chest pain after an adulterous intercourse with a young woman. At echocardiography a typical apical ballooning phenomenon was detectable and completely reversed after one week. Coronary angiography did not show significant coronary atherosclerosis.

WereadwithgreatinterestthepaperbyShaoet al.highlightingthepossible shared mechanism underlying McConnell's phenomenon andreverseTakotsubocardiomyopathy(TTC)[1].Theauthorsbrilliantlyre-late ventricular wall overstretching induced by abrupt increase inafterload and transient ventricular dyskinesis observable in pulmonaryembolism (McConnell's sign [2]) with basal dyskinesis characterizingreverse TTC [3]. The authors also remarked that myocardial ischemiapossibly induced by increased local wall stress may further precipitatemyocardial stunning observable in both conditions, usually featuredby local dyskinesis and generally related to catecholamine toxicity inTTC. Tricuspid regurgitation, another condition potentially generatedby the right ventricular overload in pulmonary embolism, may be alsofound in the right ventricular TTC [4].We surely agree that abrupt increase in afterload may represent apossible link between McConnell's phenomenon and reverse TTC.Shao & colleagues, however, do hesitate to correlate McConnell's phe-nomenonalsowithapicalballooningobservedintypicalTTC,which,in-stead, the authors associate with lower ventricular afterload forms ofstress cardiomyopathy.Notwithstanding, some points should be considered for a completeassessment of the left ventricular afterload.First, catecholamine surge observed in TTC may be associated withperipheral vaso-constriction: apparently lower peripheral blood pres-sure values may therefore result deceptive and conceal rather highercentral arterial blood pressure values, which eventually determine theeffective left ventricular afterload [5].Second, dehydration, a condition often observed in TTC [6,7],mayprecipitatelatentleft intra-ventriculargradients,leadingtoleftventric-ularoutflowtractobstruction[8],intra-ventriculargradientsandfinallyextremely higher left ventricularapical afterloads,potentially responsi-ble for apical stretching and bulging found in TTC apical ballooning.Even in suchcase,peripheralarterialpressure levelsmaybeapparentlynormal and deceptively lower than the actual pressure burden on theleftventricularapex.Leftventricularwallstretchingmaycauseexternalcompression of coronary vessel in overstretched areas, thus leading tomyocardial ischemia and stunning, and further precipitating apical bal-looning.Themechanism,however,isusuallyselflimiting:leftventricu-lar dilation lowers ventricular pressure and after-load, and systolicfunction of dyskinetic areas gradually recovers.Third, left ventricular basal hyperkinesis may (sometimes?) pre-cede apical ballooning; given this event, the first ‘victims’ of the leftventricular overload may be represented by apical segments, whichare eventually overstretched and display characteristic apical bal-looning [5].In conclusion, shared underlying mechanisms linking McConnell'sphenomenon observable in pulmonary embolism and reverse basalTTC could not be actually excluded even in typical TTC with apicaldysfunction, just because of the presence of several conditionswhich can induce abrupt increase in the left ventricular apex afterload.Further studies and brilliant interpretative views, like those fromShao et al. [1], are surely deserved for the future to better address thisissue.Conflict of interestThe authors have no potential conflict of interest to disclose.

Spontaneous coronary artery dissection (SCAD) causing acute myocardial infarction is a rare event. It occurs mostly in young women without traditional risk factors for coronary artery disease, particularly during the peripartum period. We describe two occurrences of SCAD in young women in whom coronary atherosclerosis was also present. In both cases, angiography showed extended coronary dissection on the left anterior descending coronary artery (LAD), starting from an atheromasic stenosis on the middle LAD segment. Coronary dissection could complicate an unstable atheromasic plaque, especially in young women presenting with acute coronary syndrome.

Increased levels of C-reactive protein (CRP) could be detected in subjects with acute coronary syndrome (ACS). Several factors, atherosclerosis, coronary flow impairment, myocardial necrosis, each one acting during a different, earlier or later, phase of ACS, are supposed to be involved in CRP release in case of ACS. Role and relevance of each factor, not mutually exclusive, still need to be comparatively evaluated but a cooperative synergism could be presumably hypothesized.

C-reactive protein (CRP) plasmatic levels increase in patients with acute coronary syndromes (ACS). Correlations between CRP levels, myocardial functional damage and cardiomyocyte lysis remain to be defined.192 consecutive patients with acute coronary syndromes (64.97 +/- 11.08 mean age, 71.35% male gender) were included in the study; 138 patients (71.87%) were discharged with an acute myocardial infarction (AMI) diagnosis (28 with non Q-wave AMI) and 54 with an unstable angina (UA) diagnosis (28.13%). In all patients CRP, CK, LDH, CK-MB and troponin I plasmatic concentrations were evaluated every 6 h for 48 h and every 24 h for the following 2 days from the onset of symptoms. Ejection fraction was estimated by bidimensional echocardiography and extension of myocardial lysis by cardiac enzymes plasmatic release. 92 patients (67 with AMI, 25 with UA) underwent coronary-angiography. Incidence of adverse cardiac events was recorded in a 6 months follow up.Mean CRP levels in Q-wave MI showed a statistically significant increase in the different blood samples with baseline. Mean CRP levels of the three groups were not statistically different at baseline and after 6, 12, and 18 h. Q-wave AMI CRP levels showed a statistically significant difference as against non Q-wave AMI at 36 (p0.05), 48 (p0.05) and 72 h (p0.05) and UA at 24 (p0.01), 30 (p0.01), 48 (p0.0001), 72 (p = 0.0001) and 96 h (p = 0.0003); non Q-wave AMI CPR levels showed a statistically significant difference as against UA at 48 h (p0.01). CRP peak mean levels were significantly different when comparing Q-wave AMI patients with UA patients (8.21 +/- 7.85 vs. 2.75 +/- 3.33 mg/dl, p0.001). In patients with Q-wave AMI there was a correlation between CRP peak concentrations and CK (r = 0.264, p = 0.008) and LDH (r = 0.32, p = 0.001), while correlation with CK-MB peak concentrations was not statistically significant (r = 0.196, p = 0.051). In the same patient group, there was also a correlation between CRP plasmatic concentrations and troponin I plasmatic concentrations from the 30th to 96th h after the onset of symptoms (r = 0.38-0.53, p0.05). No correlation was found between CRP levels and ejection fraction and angio-coronarography findings (number of stenotic vessels, culprit lesions, ruptured plaques). Peak CRP levels were associated in a 6 months follow up with an increased incidence of major adverse cardiac events (MACEs) in patients with Q-wave AMI (HR 1.1649, 95% C.I. 1.0197-1.3307, p0.05).CRP plasmatic concentrations showed a different release curve in patients with Q-wave AMI in comparison with patients with non Q-wave AMI and with patients with UA. CRP peak concentrations did not correlate with ejection fraction and angiographic findings, but correlate with incidence of MACE. The increase in CRP levels during Q-wave MI seems to be linked to the extension of myocardial damage rather than pre-existing inflammation.

A 17-year-old adolescent woman with hypertension related to a pheochromocytoma was admitted to the intensive care unit with epigastric pain, headache, psychomotor agitation, nausea, and vomiting. Arterial blood pressure was 170/140 mmHg and heart rate was 170 bpm. The ECG showed sinus tachycardia with ST-segment elevation in anterior and inferior leads (V3–V6, DII, DIII, and aVF) (Fig. 1a and b). Trans-thoracic echocardiography unexpectedly showed severe left ventricular dysfunction (ejection fraction 20%) with apical dyskinesis and basal hyperkinesis (apical ballooning) (Fig. 1c, video 1). Troponin-I levels were mildly elevated (1.56 ng/ml, n.v. 0.03), NTBNP 8850 pg/ml (n.v. b900), urinary noradrenaline 2945 μg/24 h (n.v. b85.5), and C-reactive protein 12.28 mg/L (n.v. b5). The patient, on the basis of a prior diagnosis of pheochromocytoma, was therefore treated with alpha and beta-1-adrenergic blockers (doxazosin, esmolol). The girl gradually recovered and 7 days later was discharged with a normal ECG and echocardiography showing improved left ventricular ejection fraction (>55%) (Fig. 1d and e, video 2). The patient eventually underwent excision of the adrenal mass one month later; histology confirmed the adrenal mass to be a pheochromocytoma. Pheochromocytomas are rare neuro-endocrine catecholaminesecreting tumors with a highly variable clinical presentation but most

Tako-Tsubo (TT) syndrome is characterized by acute onset ofchest symptoms, ECG changes with elevated cardiac markers mim-icking acute myocardial infarction, left ventricular (LV) wall motionabnormalities in the apical region with preserved function of base,and normal coronary arteries [1]. Those affected are typically olderwomen presenting after a stressful trigger, either emotional orphysical.A 70-year-old woman with history of hypertension, diabetes,asthma and allergy, was admitted with chest pain and dyspnea,whichsuddenly appearedafter asingle 1 g doseof ceftriaxonei.m.as-sumed because of cough and fever. On physical examination, bloodpressure was 120/70 mm Hg, heart rate 110 bpm, respiratory rate22 breaths/min, and diffuse bilateral wheezes were found. ECGshowed sinus rhythm and mild ST-elevation in anterior leads(Fig. 1a); troponin-I levels were increased (1.09 m ng/ml (n.v.b0.03)). Trans-thoracic echocardiogram showed LV systolic dysfunc-tion (ejection fraction [EF] 25%) with both apical dyskinesis andbasal hyperkinesis (Fig. 1c), and right ventricular (RV) apical dyskin-esis (Fig. 1d). Mild mitral regurgitation and tricuspid regurgitationwere also detectable at color Doppler analysis. Total IgE circulatinglevels were increased (1270 I.U./ml (n.v. b240 I.U./ml). Coronary an-giography showed normal coronary arteries and confirmed LV apicalballooning (Fig. 1e–f). Medical treatment with furosemide,levosimendan,ramipril,andbisoprololwasthereforestarted.Thepatientgradually recovered, and was discharged a week later, when all ECGanomalies, after transient onset of negative T-waves ( Fig. 1b) disap-peared. Pre-discharge echocardiography showed both improved LV (EF55%) and RV systolic functions.We report a case of transient apical ballooning triggered by admin-istration of antibiotics (cephalosporin). We therefore hypothesize thatallergic activation induced by antibiotic and featured by increased IgElevels may be related to TT phenomenon, as previously reported [2].RV apical ballooning, as found in this patient, was reported in 25% ofcases with TT syndrome [3].The exact mechanism leading to transient apical systolic dysfunc-tion is still not well elucidated. Increased catecholamine levels werethoughas responsible [4] , but also coronaryspasm has been reportedin subjects showing TT phenomenon [5].Several prior reports linked TT syndrome to bronchial asthma [6]anaphylactic reaction [7,8] and even cephalosporin administration[9], although in all these cases apical systolic dysfunction usually fol-lowed administration of i.v. epinephrine. We therefore postulate inthis patient a catecholamine independent pathway leading to TT phe-nomenon. Direct histamine effect consequent to allergic activationmay be presumed as responsible for transient apical dysfunction.Two cases of profound reversible myocardial dysfunction occurring inthe setting of anaphylaxis, with histamine discussed as a potential myo-cardial depressor, were previously reported [10]. Raper et al. noted thatstimulation of histamine receptors in both animal and human hearts ex-perimentally leads to myocardial depression, providing a possibleexplaining mechanism for our findings.References