Morning hours are the period of the day characterized by the highest incidence of major cardiovascular events including myocardial infarction, sudden death or stroke. They are also characterized by important neurohormonal changes, in particular, the activation of sympathetic nervous system which usually leads to a rapid increase in blood pressure (BP), known as morning blood pressure surge (MBPS). It was hypothesized that excessive MBPS may be causally involved in the pathogenesis of cardiovascular events occurring in the morning by inducing hemodynamic stress. A number of studies support an independent relationship of MBPS with organ damage, cerebrovascular complications and mortality, although some heterogeneity exists in the available evidence. This may be due to ethnic differences, methodological issues and the confounding relationship of MBPS with other features of 24-hour BP profile, such as nocturnal dipping or BP variability. Several studies are also available dealing with treatment effects on MBPS and indicating the importance of long-acting antihypertensive drugs in this regard. This paper provides an overview of pathophysiologic, methodological, prognostic and therapeutic aspects related to MBPS.

There is a paucity of data about mid-term outcome of patients with advanced heart failure (HF) treated with left ventricular assist device (LVAD) in Europe, where donor shortage and their aging limit the availability and the probability of success of heart transplantation (HTx). The aim of this study is to compare Italian single-centre mid-term outcome in prospective patients treated with LVAD vs. HTx. We evaluated 213 consecutive patients with advanced HF who underwent continuous-flow LVAD implant or HTx from 1/2006 to 2/2012, with complete follow-up at 1 year (3/2013). We compared outcome in patients who received a LVAD (n = 49) with those who underwent HTx (n = 164) and in matched groups of 39 LVAD and 39 HTx patients. Patients that were treated with LVAD had a worse risk profile in comparison with HTx patients. Kaplan-Meier survival curves estimated a one-year survival of 75.5 % in LVAD vs. 82.3 % in HTx patients, a difference that was non-statistically significant [hazard ratio (HR) 1.46; 95 % confidence interval (CI) 0.74-2.86; p = 0.27 for LVAD vs. HTx]. After group matching 1-year survival was similar between LVAD (76.9 %) and HTx (79.5 %; HR 1.15; 95 % CI 0.44-2.98; p = 0.78). Concordant data was observed at 2-year follow-up. Patients treated with LVAD as bridge-to-transplant indication (n = 22) showed a non significant better outcome compared with HTx with a 95.5 and 90.9 % survival, at 1- and 2-year follow-up, respectively. Despite worse preoperative conditions, survival is not significantly lower after LVAD than after HTx at 2-year follow-up. Given the scarce number of donors for HTx, LVAD therapy represents a valid option, potentially affecting the current allocation strategy of heart donors also in Europe.

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Keywords:Tako-tsubo cardiomyopathy arrhythmias intra-aortic ballon pump Tako-Tsubo cardiomyopathy (TTC) is characterized by a transient dysfunction of the left ventricular apex, often triggered by emotional or physical stress. Estimated prevalence of TTC ranges from 0.1 to 2.2% of patients with acute coronary syndrome (ACS). It usually occurs in old postmenopausal women. It often presents with chest pain and ECG changes (ST elevation in precordial leads and subsequent T wave inversion) and minimal myocardial enzymatic elevation which could mimic ACS, but in absence of coronary artery disease. Typical echocardiographic pattern shows apical-mid-ventricular akinesis and basal hyperkinesis. Acute heart failure and cardiogenic shock (CS) are the two most frequent TTC complications, but ventricular arrhythmias (VA) may also occur [1].We report a case of TTC presenting as an incessant sustained ventricular tachycardia (VT).A 81-year-old woman was brought to our emergency department with shortness of breath and chest pain. She had a history of hypertension under therapy with valsartan, amlodipine and clonidine, diabetes and hypercholesterolemia treated respectively with metformin and rosuvastatin. One year before, paroxysmal atrial fibrillation occurred and warfarin and amiodarone prophylaxis were introduced. On physical examination in emergency department the patient was conscious, with heart rate 110 beats/min and blood pressure 120/ 70 mm Hg. The electrocardiogram showed a wide-QRS tachycardia with left bundle branch block morphology compatible with sustained monomorphic VT (Fig. 1).On laboratory tests serum troponin I was 0.91 ng/mL, CKMB 9.1 ng/mL (normal values b0.01 ng/mL and b6.3 ng/mL, respectively) and potassium 3.5 mmol/L. The patient was initially treated with iv MgSO 4 and potassium, since she was already under amiodarone therapy. Four ineffective electrical shocks were delivered.In intensive care unit she was treated with iv lidocaine, diuretics, acetylsalycilic acid with persistence of VT. Overdrive transvenous temporary cardiac pacing wire was applied without benefit. Subsequently iv amiodarone was used with transitory restoration of sinus rhythm, then followed by multiple runs of sustained VT. Transthoracic echocardiography showed apical-mid-ventricular akinesis and basal hyperkinesis with left ventricular ejection fraction (LVEF) 30-35%. No coronary stenosis was found on angiography. Imaging findings, mildly elevated troponin I level despite regional kinesis alterations and normal coronary angiogram were consistent with TTC diagnosis.The day after, due to persistence of sustained VT, low dose metoprolol was added and lidocaine was reintroduced with no benefit. After few hours we observed a rapid worsening of hemodynamic status consistent with CS. Therefore, upon orotracheal intubation, intra-aortic balloon pump (IABP) was placed, with prompt interruption of VT and progressive improvement of hemodynamic conditions. 24 h later levosimendan was added to support IABP weaning off.At continuous ECG monitorin...