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Background— This study sought to validate the ability of amplitude spectrum area (AMSA) to predict defibrillation success and long-term survival in a large population of out-of-hospital cardiac arrests. Methods and Results— ECGs recorded by automated external defibrillators from different manufacturers were obtained from patients with cardiac arrests occurring in 8 city areas. A database, including 2447 defibrillations from 1050 patients, was used as the derivation group, and an additional database, including 1381 defibrillations from 567 patients, served as validation. A 2-second ECG window before defibrillation was analyzed, and AMSA was calculated. Univariable and multivariable regression analyses and area under the receiver operating characteristic curve were used for associations between AMSA and study end points: defibrillation success, sustained return of spontaneous circulation, and long-term survival. Among the 2447 defibrillations of the derivation database, 26.2% were successful. AMSA was significantly higher before a successful defibrillation than a failing one (13±5 versus 6.8±3.5 mV-Hz) and was an independent predictor of defibrillation success (odds ratio, 1.33; 95% confidence interval, 1.20–1.37) and sustained return of spontaneous circulation (odds ratio, 1.22; 95% confidence interval, 1.17–1.26). Area under the receiver operating characteristic curve for defibrillation success prediction was 0.86 (95% confidence interval, 0.85–0.88). AMSA was also significantly associated with long-term survival. The following AMSA thresholds were identified: 15.5 mV-Hz for defibrillation success and 6.5 mV-Hz for defibrillation failure. In the validation database, AMSA ≥15.5 mV-Hz had a positive predictive value of 84%, whereas AMSA ≤6.5 mV-Hz had a negative predictive value of 98%. Conclusions— In this large derivation-validation study, AMSA was validated as an accurate predictor of defibrillation success. AMSA also appeared as a predictor of long-term survival.

Background. Sympathetic activation induced by cold pressor test or cigarette smoking is accompanied by a marked reduction of radial artery distensibility. It is not known, however, whether arterial distensibility is under tonic sympathetic restraint, or whether this restraint involves arteries greater than the radial one in both normal and pathological conditions. Methods. We studied the distensibility of radial artery by continuous ultrasonographic assessment of the changes in arterial diameter over the diasto-systolic pressure range (finger pressure measurement) in eight patients with a Dupuytren disease before and 20 min after ipsilateral brachial plexus anaesthesia. We also studied ultrasonographic distensibility of femoral artery in seven subjects before and 20 min after ipsilateral subarachnoid anaesthesia, performed before arthroscopic surgery, and in five patients with claudicatio intermittens before and 1 month after ipsilateral removal of the lumbar sympathectomy chain. In all three conditions, the contralateral artery served as control. Results. The three interventions did not cause any significant alteration in blood pressure and heart rate. Radial artery distensibility was markedly increased by ipsilateral anaesthesia of the brachial plexus (+36%, P < 0.01). This was the case also for femoral artery distensibility both following ipsilateral subarachnoid anaesthesia in healthy subjects (+47%, P < 0.05) or ipsilateral sympathetic gangliectomy in patients with peripheral artery disease (+26%, P < 0.05). In all three instances, the distensibility of the contralateral artery remained unaffected. Conclusions. These data indicate that the sympathetic nervous system exerts a marked tonic restraint of arterial distensibility. This restraint involves medium-size and large muscular arteries and can also be seen in subjects with peripheral artery disease. This stiffening influence may increase the traumatic effect of intravascular pressure on the vessel wall and favour atherosclerosis.

Antiplatelet therapy is the cornerstone of the pharmacologic management of patients with acute coronary syndrome (ACS). Over the last years, several studies have evaluated old and new oral or intravenous antiplatelet agents in ACS patients. In particular, research was focused on assessing superiority of two novel platelet adenosine diphosphate (ADP) P2Y12 receptor antagonists (i.e. prasugrel and ticagrelor) over clopidogrel. Several large randomized controlled trials have been undertaken in this setting and a wide variety of pre-specified and post hoc analyses are available that evaluated the potential benefits of novel antiplatelet therapies in different subsets of patients with ACS. The aim of this document is to review recent data on the use of current antiplatelet agents for in-hospital treatment of ACS patients. For each drug or class of drugs, strong evidence and/or areas of uncertainty that warrant further research are highlighted by examining 10 subgroups of patients with ACS.

Sudden cardiac death (SCD) is the leading cause of death in the age group 20–65 years, in the western world, with an enormous social and economic impact. The majority of the cases of ventricular fibrillation (VF) occur in patients without a preexisting structural heart disease and represent the first manifestation of coronary artery disease. In most of these cases, VF occurs in the early phase of myocardial infarction (MI) and it is then called primary VF. Although several factors have been associated in various studies with primary VF a recent metaanalysis found no evidence for risk factors other than ST elevation and time from onset of symptoms. In the past several years, few studies have found that a family history of sudden cardiac death (SCD) is a risk factor for primary VF suggesting that this dramatic event may be favored by the genetic background. To explore this possibility we designed the ongoing PREDESTINATION Study, enrolling subjects under 75 years of age with a first MI complicated by primary VF and a control group of subjects with a first uncomplicated MI. Data so far available confirm the association between a family history of SCD and primary VF and suggest that hypokalemia and prolonged QT interval may favor its occurrence. The genetic analysis has already provided some interesting suggestions that will need to be confirmed by the continuation of the enrolment and joint analysis with data deriving from similar patient populations.

Background Exercise training induces cardiovascular changes that are both generalized and restricted to the microcirculation of the tissues more actively involved in the exercise itself. Whether the local effect of exercise extends to larger arteries is unknown, however. Methods In the right and left upper limb of 17 right-handed subjects performing an asymmetric training of the upper limbs (hammer throwers and baseball players) and 16 age-matched sedentary controls, we continuously measured radial artery diameter, distensibility and wall thickness by an echotracking and a beat-to-beat finger blood pressure device, Arterial distensibility was calculated by the arctangent model of Langewouters and expressed as continuous values from diastolic to systolic blood pressure. Measurements were made: (1) in baseline conditions; (2) after release from prolonged proximal ischaemia; and (3) after an increase in radial artery blood flow caused by a short (4 min) distal ischaemia to determine the endothelial involvement in the training-induced change in arterial distensibility, Results In athletes the radial artery distensibility was markedly greater in the right than in the left arm, the latter showing values slightly greater than those seen in the two arms of sedentary subjects. In both arms and groups radial artery distensibility increased markedly after prolonged ischaemia, the between arm and group differences being preserved, however. The radial artery response to distal short ischaemia was, on the other hand, similar in the two arms of the athletes, although greater in these subjects than in the sedentary ones. Radial artery wall thickness was greater in the trained than in the untrained arm of athletes, both values being greater than in sedentary subjects. Conclusions Asymmetrical training of the upper limbs is accompanied by a greater distensibility of the middle-sized arteries of the more trained side. This is not associated with asymmetrical changes in endothelial structure or function. It is associated with a greater wall thickness in the trained side, suggesting that, at least in part, a training-induced asymmetrical change in wall structure (possibly with a predominance of more distensible tissues such as elastine and smooth muscle) is responsible, (C) 2001 Lippincott Williams & Wilkins.