Incidenza, fattori di rischio ed outcome dell'insufficienza tricuspidalica traumatica dopo estrazione transvenosa di elettrocateteri ventricolari

Incidenza, fattori di rischio ed outcome dell'insufficienza tricuspidalica traumatica dopo estrazione transvenosa di elettrocateteri ventricolar

Predittori della prognosi a medio termine nei pazienti con cardiopatia ischemica cronica: ruolo delle anomalie della perfusione miocardica a riposo e da stress.

Il potere prognostico delle immagini di perfusione miocardica nei pazienti con cardiopatia ischemica è stato dimostrato sin dagli albori della cardiologia nucleare. In questo studio abbiamo cercato di valutare se le tecnologie più avanzate di cardiologia nucleare e i nuovi traccianti di perfusione mantengono questo potere prognostico, in particolare se confrontati con un percorso diagnostico completo e con i più vari indicatori disponibili nella cardiologia contemporanea. METODI: E’ stata selezionata dal nostro database una coorte di 676 pazienti consecutivi, che - per una cardiopatia ischemica nota o sospetta - sono stati sottoposti ad un percorso diagnostico completo, che comprendeva anche la gated-SPECT basale e da stress e la coronarografia. Sono stati esclusi i pazienti con infarto miocardio acuto, quelli sottoposti a precedenti interventi di bypass coronarico, affetti da ipertiroidismo conclamato o in trattamento emodialitico. Durante il follow-up (in media di 37 mesi), 24 pazienti sono deceduti per cause cardiache e 19 hanno avuto un infarto miocardico non fatale. RISULTATI: usando analisi di Cox, i predittori indipendenti della sopravvivenza libera da eventi (morte cardiaca e infarto miocardico acuto non fatale) sono stati, nelle diverse fasi del percorso diagnostico: la presenza di pregresso infarto miocardico fra le variabili cliniche, la creatininemia e il rapporto fra i livelli plasmatici di colesterolo LDL e HDL fra gli esami di laboratorio, la frazione di eiezione del ventricolo sinistro fra le variabili elettrocardiografiche e ecocardiografiche, il summed rest (SRS) e summed difference score (SDS) fra le variabili estratte dalla SPECT e l’estensione delle lesioni coronariche alla coronarografia. Quando le suddette variabili sono state valutate insieme, SRS (p .25). rendendo invece disponibile l’informazione fornita dalla gated-SPECT dopo le variabili cliniche, di laboratorio, elettrocardiografiche, ecocardiografiche e coronarografiche, la stratificazione prognostica è aumenta significativamente (p <.05). In 492 pazienti la diagnosi di cardiopatia ischemica è stata accertata; in questi pazienti SRS e SDS sono risultati i predittori finali indipendenti della sopravvivenza libera da eventi. La terapia medica e la rivascolarizzazione, mediante angioplastica o chirurgia coronarica, non hanno modificato le informazioni prognostiche fornite dalla gated-SPECT. CONCLUSIONI: I difetti di perfusione miocardica a riposo e da stress sono ancora i migliori predittori di sopravvivenza libera da eventi cardiaci in pazienti con cardiopatia ischemica accertata o sospetta anche se rapportati con un percorso diagnostico completo ed attuale

Myocardial fibrosis as a key determinant of left ventricular remodeling in idiopathic dilated cardiomyopathy: a contrast-enhanced cardiovascular magnetic study

In idiopathic dilated cardiomyopathy, there are scarce data on the influence of late gadolinium enhancement (LGE) assessed by cardiovascular magnetic resonance on left ventricular (LV) remodeling

Ozone and cardiovascular injury

Abstract Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular diseases in urban communities. The potential detrimental effects are both acute and chronic having a strong impact on morbidity and mortality. The acute exposure to pollutants has been linked to adverse cardiovascular events such as myocardial infarction, heart failure and life-threatening arrhythmias. The long-terms effects are related to the lifetime risk of death from cardiac causes. The WHO estimates that air pollution is responsible for 3 million premature deaths each year. The evidence supporting these data is very strong nonetheless, epidemiologic and observational data have the main limitation of imprecise measurements. Moreover, the lack of clinical experimental models makes it difficult to demonstrate the individual risk. The other limitation is related to the lack of a clear mechanism explaining the effects of pollution on cardiovascular mortality. In the present review we will explore the epidemiological, clinical and experimental evidence of the effects of ozone on cardiovascular diseases. The pathophysiologic consequences of air pollutant exposures have been extensively investigated in pulmonary systems, and it is clear that some of the major components of air pollution (e.g. ozone and particulate matter) can initiate and exacerbate lung disease in humans 1. It is possible that pulmonary oxidant stress mediated by particulate matter and/or ozone (O3) exposure can result in downstream perturbations in the cardiovasculature, as the pulmonary and cardiovascular systems are intricately associated, and it is well documented that specific environmental toxins (such as tobacco smoke 2) introduced through the lungs can initiate and/or accelerate cardiovascular disease development. Indeed, several epidemiologic studies have proved that there is an association between PM and O3 and the increased incidence of cardiovascular morbidity and mortality 3. Most of the evidence comes from studies of ambient particles concentrations. However, in Europe and elsewhere, the air pollution profile has gradually changed toward a more pronounced photochemical component. Ozone is one of the most toxic components of the photochemical air pollution mixture. Indeed, the biological basis for these observations has not been elucidated. In the present review, the role of ozone as chemical molecule will be firstly considered. Secondly, pathogenetic mechanisms connecting the atmospheric ozone level and cardiovascular pathology will be examined. Thirdly, the literature relating hospitalization frequency, morbidity and mortality due to cardiovascular causes and ozone concentration will be studied. The correlation between ozone level and occurrence of acute myocardial infarction will be eventually discussed.</p

Mild thyroid dysfunction increases mortality in acute cardiac disease

The prognostic impact of mildly altered thyroid function in the setting of acute cardiac care is not well defined. The aim of the study was to assess the relationship between thyroid function and mortality in a population with a wide range of acute cardiac diseases

Persistence of Mortality Risk in Patients With Acute Cardiac Diseases and Mild Thyroid Dysfunction.

INTRODUCTION:: There are no studies on the long-term prognostic role of abnormal hyrotropin value in patients with acute cardiac diseases. Aim of the study was to assess the incidence and persistence of risk of cardiac and overall deaths in patients with acute cardiac diseases. METHODS:: A total of 1026 patients (mean age: 67.7 years) were divided into 4 groups: (1) euthyroid (EU, n = 579); (2) subclinical-like hypothyroidism (SLHYPO, n = 68); (3) subclinical-like hyperthyroidism (SLHYPER, n = 23) and (4) low-triiodothyronine syndrome (LowT3, n = 356). Follow-up started from the day of thyroid hormone evaluation (mean follow-up: 30 months). The events considered were cardiac and overall deaths. RESULTS:: Survival rate for cardiac death was lower in SLHYPO and in LT3 than in EU (log rank test; &#967; = 33.6; P < 0.001). Survival rate for overall death was lower in SLHYPO, SLHYPER and LowT3 than in EU (48.3; P < 0.001). After adjustment for several risk factors, the hazard ratio for cardiac death was higher in SLHYPO (3.65; P = 0.004) in LowT3 (1.88; P = 0.032) and in SLHYPER (4.73; P = 0.047). Hazard ratio for overall death was higher in SLHYPO (2.30; P = 0.009), in LowT3 (1.63; P = 0.017) and in SLHYPER than in EU (3.71; P = 0.004). Hazards for SLHYPO, SLHYPER and LowT3 with respect to EU were proportional over the follow-up period. CONCLUSION:: In patients with acute cardiac disease, a mildly altered thyroid status was associated with increased risk of mortality that remains constant during all the follow-up.