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Cardiovascular diseases are a major cause of premature death and disability. They represent an extraordinarily strong financial burden upon health-care systems in ‘‘developed’’ countries. Elevated blood pressure is a major cause of cardiovascular disease. There is much evidence that cardiovascular risk increases from normal blood pressure (i.e., from 115/75 mmHg upwards) [1]. Overwhelming evidence shows that reducing salt intake from 9–12 g/day to 5–6 g/day lowers blood pressure [2]. Blood pressure is a surrogate endpoint, but may be related to a reduction of morbidity and mortality due to cardiovascular causes. Thus, intensive support and encouragement to cut down on the intake of salt in foods might reduce cardiovascular risk. Such a primary prevention strategy might significantly reduce social and health-care costs. The metaanalysis published simultaneously by Taylor et al. [3, 4] in the Cochrane Database of Systematic Reviews and the American Journal of Hypertension deals with this important issue. Specifically, it assesses the long-term effects of interventions aimed at reducing dietary salt upon morbidity and mortality due to cardiovascular causes. They found 7 studies (involving 6,489 participants) that met the inclusion criteria. Three of the seven studies focused on normotensive subjects; two on hypertensives; one in a mixed population of normotensives and hypertensives; and one in subjects with heart failure (n = 232). Despite the large number of collated cardiovascular events (665 deaths in 6,250 participants), the meta-analyses fails to show significant differences in intervention groups compared with controls. There is only limited evidence that dietary advice to reduce salt intake may increase the prevalence of deaths in people with heart failure [relative risk at the end of the trial: 2.59; 95 % confidence interval (CI), 1.04–6.44; 21 deaths]. The authors conclude that there is insufficient power to exclude the clinically important effects of reduced dietary salt on mortality or cardiovascular morbidity in normotensive or hypertensive populations. Moreover, they state that further evidences from randomized controlled trials would be needed to confirm if the restriction of dietary sodium is harmful for people with heart failure. In a recent comment, two preventive-medicine experts, Dr. He and Professor MacGregor [5], criticize the metaanalysis published by Taylor et al. [3, 4]. In their opinion, meta-analysis ‘‘reflects poorly on the reputation of the Cochrane Library and the authors’’. The two experts make statements regarding the fact that one trial in heart failure did not have to be included in the meta-analysis; they claimed that the trial was clinically heterogeneous. Indeed, patients who had been included in that trial were severely depleted of salt and water due to aggressive diuretic therapy. Moreover, the experts re-analyzed the data by combining together the results for hypertensive and normotensive subjects. Their results show a significant reduction in cardiovascular events by 20 % (pooled relative risk: 0.80; 95 % CI, 0.64–0.99). The meta-analysis was undertaken using the fixed-effect model because the heterogeneity among studies did not reach the standard probability value for significance. However, this could be the case of ‘‘not practicing what you preach’’. Despite accepting statistical homogeneity according to Cochrane’s Q test (p = 0.36) and the low value of the I index (only 6 % diversity among trials was detected), pooling data from two populations (hypertensives and normotensives) S. Corrao (&) L. Calvo G. Licata Centre of Research for Effectiveness and Appropriateness in Medicine (C.R.E.A.M.), Biomedical Department of Internal Medicine and Subspecialties, University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy e-mail: s.corrao@tiscali.it

A 39-year-old man presented to the emergency department (ED) of the ‘‘Paolo Giaccone’’ Academic Hospital, Palermo (Italy). He had anterior chest pain that did not radiate to the neck or arms. The patient came from home where the chest pain initiated. The patient was morbidly obese (BMI 54 kg/m). At the ED, the patient’s blood pressure was 120/80 mmHg, the serum troponin I concentration was 0.029 ng/ml (normal values \ 0.034, borderline 0.034–0.12), myoglobin 45 ng/ml (normal values \ 120). While experiencing chest pain, the patient underwent a standard 12 lead electrocardiogram (ECG) that was normal. An echocardiogram, also during the chest pain, excluded the presence of hypo-akinetic left ventricle areas. He was admitted to the internal medicine ward of the same hospital for clinical monitoring. Cardiac biohumoral markers were measured every 4 h, and were always within normal range (only troponin I reached 0.12 ng/ml falling to 0.028 ng/ml). On the following morning, anterior chest pain recurred. Another ECG was performed, but showed no abnormalities (Fig. 1a). During the afternoon, the patient underwent another ECG. He had no thoracic discomfort or pain, but the ECG showed a biphasic T wave inversion in V2–V6 precordial leads (Fig. 1b). Cardiac markers resulted again within normal range. An internal medicine resident who was trained to manage uncommon clinical pictures by PubMed searching [1] recognized this abnormal pattern (ECG abnormalities in an asymptomatic patient with prior anterior chest pain) performed a PubMed search using the following simple search string (biphasic T waves AND precordial leads). Six citations were found and Wellens’ Syndrome diagnosis was suggested. An internist confirmed the diagnostic hypothesis, and the patient, was taken to the invasive hemodynamic lab. Coronary arteriography was performed showing a 95% stenosis of the left anterior descending (LAD) coronary artery (Fig. 2a). The patient underwent percutaneous transluminal coronary angioplasty with resolution of the stenosis (Fig. 2b) and was discharged after 6 days in good condition. In 1982, Wellens et al. [2] described a characteristic ECG pattern associated with a critical stenosis of the LAD coronary artery and impending myocardial infarction. Tilkian [3] was the first to use the term Wellens’ syndrome defined as a group of ECG signs that occur during the painfree period in a patient with unstable angina. These ECG abnormalities, in the absence of pathologic Q waves, are predictive of a critical proximal LAD stenosis [2, 4]. They consist of an isolectric or minimally elevated ST segment followed by a concave or straight ST segment and symmetrically inverted (or biphasic) T waves in the precordial leads, frequently in V2–V3, but sometimes involving V4, V5 or V6. [4]. This was the case of our patients who showed a biphasic T wave inversion in V2–V6, leads during a pain-free period. In conclusion, this uncommon clinical picture involves one of the four clinical diagnostic strategies known as pattern recognition. This kind of diagnostic method particularly depends upon the experience of the physician. Nevertheless, we think this kind of clinical picture could be interpreted successfully using PubMed by a non-experienced physician [5]. S. Corrao (&) S. Amico L. Calvo E. Barone G. Licata Dipartimento Biomedico di Medicina Interna e Specialistica, Universita di Palermo, Piazza delle Cliniche, 2, 90127 Palermo, Italy e-mail: s.corrao@tiscali.it

The problem of halitosis has been reported since ancienttimes. References have been found in papyrus manuscriptsdating back to 1550 BC. Hippocrates advised that any girlshould have pleasant breath, making sure always to washher mouth with wine, anise and dill seeds [1].More than50 years ago, Blackburn [2] investigated halitosis in a case-series of 73 patients affected by leukemia. He found apeculiar odor of the breath resembling that of a freshlyopened corpse. This characteristic smell is not associatedwith clinical involvement of the gum, mouth, or upperrespiratory or alimentary tract. He associated this particularsmell with the hematologic disease. Nearly 15 years ago,the role of cadaverine was pointed out as a putative com-ponent of halitosis [3]. On the contrary, putrescine, that issimilar to cadaverine, is not involved as component ofhalitosis. Cadaverine, together with putrescine, was firstdescribed in 1885 [4] by the German physician LudwigBrieger (1849–1919). Cadaverine is a toxic diamine usu-ally produced by protein hydrolysis during putrefaction ofanimal tissue. Cadaverine is also known as 1,5-pentanedi-amine and pentamethylenediamine, and represents one ofthe substances possibly implicated in establishing halitosis.Particularly, isolates of Klebsiella and Enterobacter havebeen found to emit foul odors in vitro that resemble badbreath, with concomitant production of volatile sulfides andcadaverine [5].When incubated on a sterile denture,enterobacterial isolates produce typical denture foul odor.Moreover, isolates exhibit cell-surface hydrophobic prop-erties when tested for adhesion to acryl and aggregationwith ammonium sulphate. The results, taken together,suggest that Klebsiella and related Enterobacteriaceae mayplay a role in denture malodor. However, cadaverine maybe produced by other mechanisms as well as oral bacterialgrowth.From a conventional point of view, halitosis, fetor oris,oral malodor or bad breath are the general terms used todescribe unpleasant breath emitted from a person’s mouthregardless of whether the odorous substances in the breathoriginate from oral or non-oral sources. There are fewstudies evaluating the prevalence of oral malodor in thegeneral population, with reported rates ranging from 22 tomore than 50%. In addition, approximately 50% of adultsand elderly individuals emit socially unacceptable breath,related to physiologic causes, upon arising in the morning[6]. Moreover, there are no universally accepted standardcriteria, objective or subjective that define a halitosispatient [7].Thus, this is a clinical problem as common asundervalued by clinicians who have to remember theimportance of physical examination as from the mouth’ssmell for an all-inclusive clinical decision-making. In thisissue of Internal and Emergency Medicine, Campisi et al.[8] have carried out an excellent and complete guide forapproaching the halitosis symptom. Each of us can learnfrom this interesting and in-depth review. As the authorsstate, despite its frequency, this problem is often unac-cepted and declared as taboo. However, even if nearly 90%of patients suffering from halitosis have oral causes, animportant percentage of oral malodor cases have an extra-oral etiology. They may often be referred to the category of‘‘blood-borne halitosis’’. According to the Tangerman [9]classification, this is one of the three major categoriestogether with upper respiratory tract and lower respiratorytract causes. Many organ or systemic diseases may beresponsible for ‘‘blood-borne halitosis’’ even though some