Supraventricular Tachycardia Causing Left Ventricular Dysfunction.

There is limited evidence on characterization and natural history of supraventricular tachycardia (SVT)-induced left ventricular (LV) dysfunction. The aim of this work was to characterize clinical features and long-term evolution of SVT-induced LV dysfunction. Patients consecutively admitted with sustained SVT and heart rate >100 bpm as the only known cause of a new onset LV systolic dysfunction (i.e., LV ejection fraction [EF] <50%) were analyzed. Patients were then revaluated periodically. Recovered LVEF (i.e., ≥50%) and a composite of death, heart transplant or first episode of major ventricular arrhythmias were evaluated as study end-points. We enrolled 83 patients. After SVT therapy, 56 (67%) showed a recovered LVEF at the last follow-up of median 54 (interquartile range 36 to 87) months. Seventeen (30%) of those patients had a temporary new drop in LVEF during follow-up associated to high-rate SVT relapse. At presentation, patients with recovered LVEF were younger (52 vs 67 years respectively, p <0.001) and had higher LVEF (34% vs 27% respectively, p = 0.005) compared to non-recovered LVEF patients. Finally, 4% of recovered LVEF patients vs 26% of nonrecovered LVEF patients experienced death/heart transplant/major ventricular arrhythmias during follow-up (p = 0.004). In conclusion, after almost 5 years of follow-up, two-thirds of patients with high-rate SVT causing a newly diagnosed LV systolic dysfunction recovered and maintained normal LV function after SVT control, with a subsequent benign outcome. Long term individual surveillance is required in those patients, as arrhythmic recurrences and new drops in LVEF are common in the long term.

[Nonvalvular atrial fibrillation: data from the Observatory of Cardiovascular Diseases in the province of Trieste (Italy)]. / La fibrillazione atriale non valvolare: dati dall'Osservatorio delle Malattie Cardiovascolari della provincia di Trieste.

BACKGROUND: Nonvalvular atrial fibrillation (NVAF) is the most common arrhythmia in outpatients and is associated with increased mortality, thromboembolic and hemorrhagic events. Although several international studies have evaluated its prognostic impact in the real world, Italian data are still lacking. Our aim was to define the prevalence, comorbidity, treatment and outcome in a population of "real-life" outpatients with NVAF. METHODS: From 2009 to 2013, 21 282 consecutive patients referred to the Cardiovascular Center of Trieste were enrolled in the study. NVAF was defined in the absence of moderate-to-severe valvular disease, valvular interventions, rheumatic heart disease. Events evaluated in the follow-up included mortality, hospitalizations, thromboembolism and hemorrhage. Clinical data and events were derived from the cardiac regional electronic patient records and the ICD-9 hospital discharge records. RESULTS: 3379 patients (15.8%) had NVAF (35.6% paroxysmal, 34.5% persistent, 29.9% permanent); compared to the general population these patients were older, predominantly male, with hypertension, diabetes and history of stroke/transient ischemic attack and heart failure. Oral anticoagulant therapy was prescribed in 54% of cases, above all in persistent or permanent forms, in patients with higher CHA2DS2-VASc score and younger age. The rate of all-cause mortality, cardiovascular hospitalization, thromboembolic and hemorrhagic events during follow-up was higher in patients with NVAF than in the general population. The use of oral anticoagulant therapy reduced the incidence of thromboembolic events. CHA2DS2-VASc score emerged as an independent predictor of thromboembolic events in patients with paroxysmal (35% higher risk), persistent (40% higher risk) and permanent atrial fibrillation (34% higher risk than patients without atrial fibrillation). CONCLUSIONS: In "real-life" outpatients NVAF is associated with older age, more comorbidities and increased cardiovascular events. CHA2DS2-VASc and HAS-BLED scores predict accurately the risk for thromboembolic and hemorrhagic events. Oral anticoagulation reduces thromboembolic events, but its use is limited to just half of the patients.

[Sudden cardiac death in patients with left ventricular dysfunction from ischemic heart disease: role of the implantable defibrillator. Evidence, guidelines and good clinical judgment]. / Morte cardiaca improvvisa nella disfunzione ventricolare da cardiopatia ischemica: il ruolo del defibrillatore impiantabile tra evidenze, linee guida e buon senso clinico.

A number of studies have shown that the implantable cardioverter-defibrillator (ICD) is the most effective therapy for the prevention of sudden cardiac death from ventricular arrhythmias in patients with ischemic heart disease and severe left ventricular dysfunction. However, ejection fraction should not be considered the only parameter for the identification of candidates to ICD; this may lead to a "hyper-simplification" of the choices and to often unnecessary or inappropriate implantations. The purpose of this paper was to review the literature data regarding indications for ICD implantation in primary prevention in patients with severe ischemic left ventricular dysfunction by taking into account different clinical settings, in particular the biological age, the comorbidity profile, the temporal length between the ischemic event and ICD implantation, the possible impact of revascularization in reducing the arrhythmic risk.

How can optimization of medical treatment avoid unnecessary implantable cardioverter-defibrillator implantations in patients with idiopathic dilated cardiomyopathy presenting with "SCD-HeFT criteria?".

To assess the proportion and long-term outcomes of patients with idiopathic dilated cardiomyopathy and potential indications for implantable cardioverter-defibrillator before and after optimization of medical treatment, 503 consecutive patients with idiopathic dilated cardiomyopathy were evaluated from 1988 to 2006. A total of 245 patients (49%) satisfied the "Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) criteria," defined as a left ventricular ejection fraction of ≤0.35 and New York Heart Association (NYHA) class II-III on registration. Among these, 162 (group A) were re-evaluated 5.4 ± 2 months later with concurrent ß-blockers and angiotensin-converting enzyme inhibitor use. Of the 162 patients, 50 (31%) still had "SCD-HeFT criteria" (group A1), 109 (67%) had an improved left ventricular ejection fraction and/or New York Heart Association class (group A2), and 3 (2%) were in NYHA class IV. Of the 227 patients without baseline "SCD-HeFT criteria" (left ventricular ejection fraction >0.35 or NYHA class I), 125 were evaluated after 5.5 ± 2 months. Of these 227 patients, 13 (10%) developed "SCD-HeFT criteria" (group B1), 111 (89%) remained without "SCD-HeFT criteria" (group B2), and 1 (1%) had worsened to NYHA class IV. The 10-year mortality/heart transplantation and sudden death/sustained ventricular arrhythmia rate was 57% and 37% in group A1, 23% and 20% in group A2 (p <0.001 for mortality/heart transplantation and p = 0.014 for sudden death/sustained ventricular arrhythmia vs group A1), 45% and 41% in group B1 (p = NS vs group A1), 16% and 14% in group B2 (p = NS vs group A2), respectively. In conclusion, two thirds of patients with idiopathic dilated cardiomyopathy and "SCD-HeFT criteria" at presentation did not maintain implantable cardioverter-defibrillator indications 3 to 9 months later with optimal medical therapy. Their long-term outcome was excellent, similar to that observed for patients who had never met the "SCD-HeFT criteria."

Predictors for restoration of normal left ventricular function in response to cardiac resynchronization therapy measured at time of implantation.

There are no parameters predicting the individual probability of "full response" to cardiac resynchronization therapy (CRT). The aim of this work was to find prognostic factors of full clinical and echocardiographic responses (i.e., ≥50% left ventricular ejection fraction [LVEF] and New York Heart Association class I) after 1 year of CRT. This was a prospective follow-up study that involved 2 hospitals. Patients (n = 75) with advanced heart failure (64 ± 9 years of age, 87% men, LVEF 24 ± 7%) who received CRT were followed for 17 ± 9 months. Univariate and multivariate regression analyses were used to identify predictors of full CRT response. A nomogram predicting the individual probability of full CRT response during follow-up was calculated. There were 13 patients with restoration of normal LVEF versus 62 without (mean LVEF 56% ± 5% vs 31% ± 8%, respectively, p <0.001). Predictors of full response included cause of heart disease, baseline QRS width, and degree of QRS shortening in response to CRT. Patients with nonischemic heart disease, baseline QRS width ≤150 ms, and QRS shortening ≥40 ms in response to CRT had a >75% probability of restoration of normal LVEF. In conclusion, our nomogram using a combination of cause, baseline QRS width, and degree of QRS shortening in response to CRT allows assessment of individual probability of full response. This observation awaits further confirmation from larger series.

[If heart failure or cardiac arrest complicate pregnancy and delivery]. / Quando lo scompenso o l'arresto cardiaco complicano la gravidanza ed il parto.

Physiological adaptation to pregnancy exposes mother's cardiovascular system to relevant hemodynamic overload. These changes and other specific conditions of pregnancy, such as amniotic embolism, can point out unrecognized preexisting heart disease or, in the presence of some cofactors, be burdensome even for healthy hearts. Thus, tragic cases of heart failure or cardiac arrest may occur, whose management requires several considerations with respect of trying to save two lives at the same time, the need for drugs potentially harmful to the fetus, and assessment of emergent cesarean section.

[Drugs and athletic activity: do they fit together?]. / Quanto sono compatibili i farmaci con l'attività atletica.

Competitive sports eligibility, mandatory for the Italian law in all age classes, from young to master athletes, involves millions of subjects, who are at risk during their sport career both for prescription and illicit drugs (or banned substances included in the World Anti-Doping Agency list, annually updated). These drugs may interfere with adrenergic hyperactivation related to athletic activity and can bring to unfavorable cardiovascular effects, such as arrhythmias, coronary artery disease, myocarditis, pericarditis, heart failure, ion channel disease. Moreover, numerous compounds may reduce athletic performance. Cardiovascular side effects are more frequently reported when drug co-administration is performed, which occurs frequently. Drug co-administration may have a higher risk when a common metabolic pathway is used (i.e. P450 hepatic cytochrome), and inhibition or induction effects modify plasma drug levels. One of the most important problems remains for combination of drugs that might be torsadogenic. Therefore, it is mandatory to be aware of pharmacokinetic properties, mechanisms of action, side effects and interactions between drugs and competitive sports activities; moreover, possible clinical, instrumental (i.e. ECG) or laboratory markers should be pointed out in order to recognize a possible toxic effect and subsequently interrupt or modify drug administration and/or assumption.

The plasma concentration of Lpa-I:A-II particles as a predictor of the inflammatory response in patients with ST-elevation myocardial infarction.

OBJECTIVE: To investigate the relationship between plasma HDL at admission and the extent of the inflammatory response during an ST-elevation myocardial infarction (STEMI), and to analyse structural HDL changes during STEMI as related to the extent of inflammation. METHODS AND RESULTS: CRP and IL-6 were monitored for 96h in 45 patients with STEMI. Plasma apoA-II and LpA-I:A-II levels at admission, but not HDL cholesterol or other HDL-related biomarkers, were associated with the extent of the inflammatory response during STEMI, as indicated by the positive correlations with CRP AUC (apoA-II: F=7.44, p=0.009; LpA-I:A-II: F=14.29, p<0.001), and IL-6 AUC (apoA-II: F=6.98, p=0.012; LpA-I:A-II: F=6.67, p=0.013). By multivariate analysis the plasma LpA-I:A-II level at admission was a powerful independent predictor of the inflammatory response, evaluated either as CRP AUC (F=22.30, p<0.001), or IL-6 AUC (F=6.92, p=0.012). During STEMI, the plasma concentration of LpA-I:A-II, but not LpA-I particles decreased, HDL became larger and progressively enriched in serum amyloid A; these changes occurred only in patients with a significant inflammatory response. CONCLUSION: An elevated plasma concentration of LpA-I:A-II particles was an independent predictor of a more severe inflammatory response in patients with STEMI.

Syncope in a patient presenting to the emergency room with chest pain, shock, and neurological disorders.

Transient left ventricular dysfunction associated with apical ballooning at echocardiography or angiography has been described in many overlapping clinical settings: neurological disorders, such as subarachnoid haemorrhage and stroke, pheochromocytoma, and the recent takotsubo syndrome. We describe the case of an elderly woman presenting with syncope, chest pain, electrocardiographic abnormalities, mild enzymatic release, and transient left ventricular apical ballooning, mimicking an anterior wall acute coronary syndrome with shock, following a subarachnoid haemorrhage that could not be detected upon admission.The pathophysiological mechanisms of myocardial damage during catecholamine surge cannot be completely explained by epicardial coronary vasoconstriction or microvascular spasm and subsequent ischaemia; also direct catecholamine-mediated myocyte injury may play a role in myocardial stunning.

Illicit drugs and cardiac arrhythmias in athletes.

The current management of athletes with cardiac arrhythmias has become complicated by the widespread use of illicit drugs, which can be arrhythmogenic. The World Anti-Doping Agency annually updates a list of prohibited substances and methods banned by the International Olympic Committee that includes different classes of substances namely, anabolic androgenic steroids, hormones and related substances, beta2-agonists, diuretics, stimulants, narcotics, cannabinoids, glucocorticosteroids, alcohol, beta-blockers and others. Almost all illicit drugs may cause, through a direct or indirect arrhythmogenic effect, a wide range of cardiac arrhythmias (focal or reentry type, supraventricular and/or ventricular) that can even be lethal and which are frequently sport activity related. A large use of illicit drugs has been documented in competitive athletes, but the arrhythmogenic effect of specific substances is not precisely known. Precipitation of cardiac arrhythmias, particularly in the presence of a latent electrophysiologic substrate including some inherited cardiomyopathies, at risk of sudden death or due to long-term consumption of the substances, should raise the suspicion that illicit drugs may be a possible cause and lead cardiologists to investigate carefully this relationship and appropriately prevent the clinical consequences.

Congenital complete atrioventricular block in the early pediatric population.

Congenital complete atrioventricular block (CCAVB) is a rare potentially lethal disease with an estimated incidence of 1 every 15.000 to 20.000 live born infants.IN STRUCTURALLY NORMAL HEARTS TWO KINDS OF CONGENITAL HEART BLOCK CAN BE IDENTIFIED: one usually diagnosed in utero associated with the circulating maternal anti-SS-A/Ro and anti-SS-B/La antibodies, the other kind is detected later in the neonatal period or during the infancy or childhood and present no clear relation with maternal antibodies. Nowadays, the diagnosis can be made in utero as early as between week 16 and 28 of gestation by foetal echocardiography.The mortality in isolated CCAVB is estimated between 8 and 16% and between 4 and 8% in children and adults. The mortality and morbidity of patients diagnosed outside the neonatal period is significantly lower than those with a in utero diagnosis.Risk factors for worse outcome in CCAVB are the foetal diagnosis, the presence of hydrops fetalis, delivery at 32 weeks gestation, and a ventricular rate <55 beats/min in early pregnancy (13,18).Aim of this review is to delineate the current knowledge on CCAVB presenting in children without structural heart disease including aetiology, outcome and management. Also outlined in this review are some of the problems still debated in this issue.