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We report the case of a 75-year-old man, referred for worsening dyspnea and fever. The electrocardiography (ECG) showed mild ST-elevation in anterior leads, while cardiac echography severe left ventricular (LV) systolic dysfunction with apical ballooning. Later on, ECG showed negative T-waves and QT-prolongation in the same anterior leads and T-waves positivization during fever peak. Ten days later, LV ejection fraction completely recovered, apical ballooning and fever disappeared. We, therefore, hypothesize that transient apical ballooning found in our patient may have been induced by a respiratory infection, not detectable at seriate blood cultures.

We report a case of 46 year-old man, admitted to our Department for a possible massive pulmonary embolism. Instead, diagnosis of Tetralogy of Fallot was established by echocardiography and cardiac catetherization.

A 68-year-old man with anterior ST-elevation acute myocardial infarction was treated with primary angioplasty of the proximal left anterior descending (LAD) artery. Coronary angiography showed coronary atherosclerosis and a rare combination of congenital coronary anomalies on other coronary vessels (myocardial bridge on mid-LAD and ectopic origin of the circumflex coronary). Coronary angioplasty on the ectopic circumflex was therefore required.

We report the case of a 72-year-old man with ST-elevation acute myocardial infarction and severe intra-ventricular gradient (>40 mmHg), who died with left ventricular rupture (LVR). We postulate that severe intra-ventricular gradient detectable at admission may be related to subsequent LVR and proposed as a risk factor for LVR.

We describe the case of a 22-year old woman affected by familial hypercholesterolemia, referred for chest pain and treated with angioplasty of left anterior descending coronary artery. Marked systemic inflammation associated with acute coronary syndrome was reduced by 1-month therapy with high dose atorvastatin.

We investigated the presence of Chlamydophila pneumoniae antibodies in 125 patients with cardiovascular disease and in 128 controls. C. pneumoniae antibodies were measured by microimmunofluorescence assay. A significantly high prevalence of IgG C. pneumoniae antibodies at titreor = 8 was found in patients (84%) in comparison to controls (47.6%). Considering as cut-off the IgG titreor = 32, 52% of patients with coronaropathies and 18.75% of controls resulted positive (p0.0001). IgA C. pneumoniae antibodies were found in patients and controls without statistically significant differences. High C. pneumoniae antibodies (titreor = 256) were found in 11% of patients with acute myocardial infarction (AMI) and in none of the controls. In patients, the percentage of IgG and IgA seropositivity increased with age and decreased in patients aged70 years. Only patients with AMI are at risk of having antibodies against C. pneumoniae (OR = 6.69). None of the known risk factors for cardiovascular disease was significantly associated with C. pneumoniae seropositivity IgG. This is the first report in our area on the possible association of C. pneumoniae IgG seropositivity and acute ischemic events.

We report the case of a 56-year-old woman with effort angina, dyspnea and a septal mass causing atrioventricular block, treated with pacemaker implantation, and left ventricular outflow tract obstruction (induced by septal mass protrusion into left ventricular cavity).

The application of tissue Doppler imaging (TDI) has shown remarkable growth in clinical practice during the past few years, especially, in risk stratification of patients with coronary heart disease or heart failure (systolic and diastolic). Myocardial performance index (MPI) is a Doppler echocardiographic parameter defined as the sum of the isovolemic contraction and relaxation times divided by the ejection time. It is considered as a reliable parameter to assess global left ventricular function. Cardiac time intervals and MPI have also been found as new applications in diagnosing cardiotoxicity from chemotherapy, COPD, valvular heart disease, pulmonary hypertension and endocrinopathies.

The aim of this study is to investigate the release of some inflammatory cytokines (Cks) during the very early phase (first 24 h) of acute coronary syndrome (ACS). Twenty-six consecutive subjects admitted to coronary care unit with ACS underwent serial blood sampling in order to evaluate concentrations of interleukin (IL)-2, IL-10, IL-18, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ. Blood samples were taken within 6 h after onset of chest pain (T0), at 12 h (T1), and at 24 h (T2). Patients were thus divided into four groups comparing pro-inflammatory Ck release (IL-2, TNF-α, and IFN-γ) and anti-inflammatory activity (IL-10). Clinical features, risk factors, incidence of adverse events, and coronary angiography findings were compared with Ck activation. Ck levels were significantly increased if compared with baseline. Subjects with marked inflammatory response showed a higher incidence of left anterior descending coronary disease (IL-2, p < 0.001; TNF-α and IFN-γ, p < 0.05) and more often incurred early complications (IL-2, p < 0.05; IFN-γ, p < 0.001). A correlation was detectable between IL-18 levels and myocardial enzyme release (creatine kinase, r = 0.47; lactate dehydrogenase, r = 0.54; troponin I, r = 0.58; p < 0.05). TNF-α levels were associated with a worse prognosis at follow-up (Log rank, p < 0.05). A Ck activation characterizes the early phase of ACS. Early inflammatory reaction seems to correlate with coronary disease and adverse events.

Tremendous advances have been made in understanding the pathophysiology and treatment of congestive heart failure (CHF). However, diagnosis still remains difficult, even with a comprehensive physical examination. Symptoms such as dyspnea are non-specific and poorly sensitive indicators for early CHF that can be largely undetected. The discovery of natriuretic peptides (BNP) as diagnostic biomarkers has been one of the most critical advances for heart failure diagnosis. Therefore, both B-type and N-terminal pro-B-type have potential role in the diagnosis of heart failure, as well as in prognostic risk assessment. A single determination of BNP at any time during the progression of chronic HF provides a clinically useful tool for risk stratification. The hypothesis that repeated measurements might carry prognostic information beyond a single measure was confirmed in different settings. One of the main interests is given to the values of repeated determinations for monitoring progression of disease, and for the evaluation of the clinical effects of medical therapy. Nevertheless, despite thousands of papers describing their potential utility, current guidelines have not endorsed the highest level of recommendation for their use, in part, because the application in clinical practice is often limited for the absence of well codified cut off. Recently, European guidelines emphasized the role of natriuretic peptides as potential laboratory markers. In the near future, algorithm building will take into consideration clinical and echocardiographic parameters as well as NP measurements, and this may lead to a correct diagnosis and identification of patients at high risk. The purpose of this review is to discuss the clinical approaches and future applications of natriuretic peptides in heart failure and coronary disease.

To evaluate levels of carbohydrate antigen-125 (CA-125) in patients with acute coronary syndrome (ACS), with regard to incidence of acute heart failure (AHF) and levels of brain natriuretic peptide (BNP).In 47 consecutive patients with ACS, circulating levels of CA-125 and BNP were ascertained in the first 24 h and after 3 days of hospitalization. Left ventricular function and in-hospital incidence of AHF were also evaluated.BNP and CA-125 levels were significantly higher in patients with pulmonary oedema (PO) (564.25+/-500.50 vs. 258.57+/-284.81 pg/ml, P0.05; 51.78+/-54.71 vs. 13.78+/-12.01 UI/ml, P0.001) proportionally to Killip class (r=0.44, r=0.47; P0.01) and were related to LV end-diastolic dimension (r=0.47, P0.01; r=0.66, P0.001) and LV ejection fraction (r=-0.63, P0.001; r=-0.37, P0.01). CA-125 levels identified patients with PO with higher specificity (97.1 vs. 31.4%), positive predictive value (83.3 vs. 33.3%) and accuracy (83.0 vs. 48.9%) when compared with BNP.CA-125 levels are increased in patients with ACS and systolic dysfunction or AHF. Patients with PO are better identified by combined BNP and CA-125 assay rather than by only BNP.

Excessive and chronic ethanol consumption exerts deleterious and diffused effects on the myocardium, independent of coronary atherosclerosis, arterial hypertension, valvular disease or congenital heart disease. Although the effects of chronic alcoholism on systolic cardiac function are well known, diastolic involvement has been evaluated only partially. This short review summarizes the experimental and clinical evidence for alcohol-induced cardiac disease.

We report the case of a 75-year-old woman with new onset dyspnoea, hypotension, and right bundle branch block. Transthoracic echocardiography (TTE) showed a thrombus in the right pulmonary artery and acute pulmonary embolism was diagnosed. The patient immediately underwent fibrinolysis with tenecteplase, with prompt recovery of clinical conditions and ECG anomalies. Bedside TTE might be helpful for immediate diagnosis of massive PE needing rapid treatment by fibrinolysis.

The membranes of left atrial appendage (LAA) cavity are very rare entity. To date, only five cases of a membrane involving LAA have been described. In this report, we describe two different cases: in Case 1, we show image of a "real" nonobstructive membrane within the body of LAA, but in Case 2 we show a linear image, mimicking a membrane within the body of LAA. It really is a "pitfall" of transesophageal echocardiography (TEE).

A 45-year-old woman was admitted to our cardiology department for palpitations and dyspnoea. She had previously been investigated by echocardiography several times, resulting in a diagnosis of hypertrophic cardiomyopathy. However, a congenitally corrected transposition of the great arteries was diagnosed by our echocardiographic examination. The patient underwent electrophysiological evaluation and the accessory pathway was successfully ablated by applying radiofrequency pulses. This case report identifies that in patients with congenitally corrected transposition of the great arteries the primary diagnosis by echocardiography can sometimes be missed and that these patients are increasingly liable to develop Congestive Heart Failure with advancing age. In order to avoid diagnostic mistakes, more widespread dissemination of information about this congenital heart defect is essential.

We read with great interest the review by Scholzel et al. [1], about chronic thromboembolic pulmonary hypertension (CTEPH), and especially, the sections on pathophysiology, risk factors and diagnostic work-up. However, we would like a further comment about congenital abnormalities causing hypercoagulability in these subjects. In fact, in our experience [2, 3], we have observed CTEPH patients with methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism or combined deficiency of proteins C and S. Can we consider these abnormalities as predisposing factors for CTEPH? Should thrombophilia screening be performed in subjects with suspect PAH? Could these abnormalities play a role in recurrent pulmonary hypertension after pulmonary endarterectomy?

Investigation of the mechanisms of atherosclerosis has determined that inflammation plays a central role in the development, progression, and outcome of acute coronary syndrome. Although C-reactive protein will remain over time a useful marker, cytokines will continue to be studied in order to understand the mechanisms of acute coronary syndrome and cytokine balance. This short review summarizes the experimental and clinical evidence regarding the role of some cytokines in acute coronary syndrome (interleukin [IL]-8, IL-10, IL-18, IL-2, tumor necrosis factor-alpha, interferon-gamma).

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.

We report a case of a baby with Down Syndrome and history of a corrective surgery for a duodenum stenosis, which was subjected to a parenteral nutrition with central venous catheter. A two-dimensional color Doppler echocar- diographic examination revealed a voluminous oval-shaped mobile inhomogeneous mass adhering to the tricuspid valve. The intraoperative pathology showed that it was a large fungal vegetation. The probable source of Candida Albicans was an infected intravenous catheter. We wish to remark the role of echocardiography in the diagnosis and choice of timing of surgery.

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

There is an increasing body of evidence that links Chlamydia pneumoniae infections to atherosclerosis and the clinical complications of unstable angina, myocardial infarction and stroke. Several epidemiologic reports indicate an association between the presence and titer of Chlamydia pneumoniae antibodies and atherosclerosis and its complications. Other studies show the presence of Chlamydia pneumoniae, chlamydial antigens or nucleic acid in atherosclerotic plaques. Moreover, experimental studies present mechanisms by which Chlamydia pneumoniae may play a role in the induction of atherosclerosis and its complications. Finally, many studies have evaluated the effect of antibiotic treatment on cardiovascular events in humans. This article reviews all the aspects that link Chlamydia pneumoniae to atherosclerosis and its clinical manifestations.

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

A 41-year-old man, with a history of non-ischaemic dilated cardiomyopathy (DCM) and an automatic implantable cardioverter defibrillator (AICD), was admitted to our Department for worsening of heart failure. During the hospitalisation, his clinical status worsened with severe hypotension and dyspnoea. Transthoracic (Fig. 1) and transoesophageal echocardiography (Fig. 2), showed a mobile thrombus in the right atrium (RA), attached to the permanent transvenous lead. A chest CT was performed and it was indicative of massive pulmonary embolism. Anticoagulation therapy was performed and the patient's clinical status improved. Fig. 1 Transthoracic echocardiography: detail of the right atrium (RA) with thrombus (T) adherent to lead Fig. 2 Transoesophageal echocardiography: detail of the right atrium (RA) with thrombus (T) adherent to lead. The mass is shown better than with transthoracic examination Thrombotic complications after implantation of pacemaker (PM) or AICDs regard essentially the veins involved in the introduction of the catheters [1]. Rarely thrombi in RA and/or pulmonary embolism secondary to permanent cardiac pacing are reported [2, 3]. This case shows that worsening of symptoms of cardiac failure, in patients with DCM and AICD, could sometimes be caused by pulmonary embolism due to an intracardiac device.

Background: Tissue Doppler Imaging (TDI) may be useful in identifying subjects at higher risk among patients with Chronic Heart Failure (CHF). The clinical role of new developed TDI parameters, however, still need to be documented. Methods: A total of 113 consecutive patients with CHF enrolled in the daunia Heart Failure Registry underwent echocardiography assessment and were followed prospectively for a mean 234±262. days. Conventional echocardiography and TDI parameters were calculated. We have also calculated peak myocardial acceleration during isovolumic relaxation time (pIVA(r)) derived from TDI (peak velocity during isovolumic relaxation (pIVV(r))/Acceleration Time (AT)). Results: Subjects readmitted for worsening HF were characterized by lower levels of pIVA(r) (0.8±0.3 vs 1.3±0.5 m/s2, p

We read with great interest the article by Fassio et al. [1] which provided a detailed review on Kounis syndrome (allergic acute coronary syndrome). The authors approached the issue both from the cardiologist’s and the allergist’s view. Authors report that initial descriptions of Kounis syndrome were focused on patients with ‘‘angiographycally’’ normal coronary arteries and acute release of allergic mediators (histamine or leukotrienes); the prognosis of these patients is good, with the left ventricular function normalizing over 3 days to several weeks [2]. However, we recently reported a case (a 70-year-old woman) of transient apical ballooning (Tako-Tsubo syndrome) [3], with mild ST-elevation in anterior leads and increased troponin-I levels [1.09 ng/ml (n.v. \ 0.03)], triggered by administration of antibiotics (cephalosporin) in a patient with history of asthma and allergy. Tako-Tsubo syndrome is characterized by acute onset of chest symptoms, ECG changes with elevated cardiac markers mimicking acute myocardial infarction, left ventricular wall motion abnormalities in the apical region with preserved function of base, and normal coronary arteries [4]. Those affected are typically older women presenting after a stressful trigger, either emotional or physical. According to authors’ opinion, could there be a link between Kounis syndrome’s variant with ‘‘angiographycally’’ normal coronary arteries and Tako-Tsubo syndrome triggered by administration of drugs in patient with history of asthma and allergy?

Dear Sir, We read with interest the article by Hoendermis [1] concerning an update on pulmonary arterial hypertension (PAH). This paper pays particular attention to the diagnosis and treatment of PAH; however, we would like to highlight the role of stress echocardiography to detect pulmonary vascular disease (PVD) prior to a rise of pulmonary arterial pressure (PAP) at rest. In fact, stress echocardiography has been successfully used on relatives of patients with idiopathic and familial PAH in a large multicentre study [2] and in patients with systemic sclerosis [3, 4]. It seems to be a useful tool to detect PVD early, but it requires further validation because of the lack of standardisation in the exercise protocol and because the cut-off value of PAP as in these cases has not been established; neither, to our knowledge, has the influence of age, gender, and body mass index on PAP been clearly defined. Stress echocardiography, despite MRI and CT, is more available and less expensive, and it might give more information on the functionality. However, today, it is not yet recommended as a routine method for the early detection of PVD, but we do hope that future research would fill the existing gaps and allow an extended use.

With great interest we read and appreciate the comments made by Dr Troise with regard to our report entitled ‘Voluminous mycetoma in a newborn with Down Syndrome: role of echocardiography’.1 He highlights positive collaboration they had set up, at that time, offering cardiac surgical treatment to the patient referred by Hospital OO.RR of Foggia. At that time, a tele-echocardiographic counselling was promptly requested. This …