1,721,141 research outputs found
Endothelial progenitor cells and long-term prognosis in patients with stable angina treated with percutaneous coronary intervention--reply
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[Management of acute chest pain in the emergency department]
No full textAcute chest pain is one of the most common symptoms in emergency departments. Immediate assessment is mandatory on arrival in order to ensure the appropriate care. Diagnostic work-up should be based on conventional tools, i.e. clinical presentation, physical examination, electrocardiogram, as well as on modern information, i.e. biochemical markers of myocardial damage or provocative tests. Firstly, physicians should assess the likelihood that signs and symptoms have a cardiac origin secondary to coronary artery disease. Afterwards, the risk for ischemic complications should be stratified. To this end, several scores have been derived from clinical trials in order to improve prediction of outcome. Also, use of critical pathways can improve guideline adherence. In the "real world", a variety of barriers to optimal management of acute chest pain still exists. An agreement on specific protocols is often difficult to achieve between different specialties. Also, no official guidelines on low-risk chest pain patients or patients with non-cardiac chest pain are available. Finally, the minimal data set of diagnostic tools that should be applied in case of acute chest pain in any emergency setting is still lacking
Acute neurological dysfunction. the missing link in the pathophysiology of takotsubo syndrome
No full textTakotsubo and brain activatio
Medical research could soon be jeopardized by new european union data protection regulations
No full textBack to the future. the crucial role of clinical registries in the era of randomized controlled trials for identifying the optimal medical therapy of heart failure
Full text linkThe elusive link between sex hormone levels and takotsubo syndrome
No full textThe higher incidence of cardiovascular disease in men than in women of similar age and the menopause-associated increase in heart diseases in women have led to the belief that gender-related differences in sex hormones might affect the development and evolution of several cardiovascular conditions [1], including coronary artery disease, valvular heart disease, and cardiomyopathies. The well-recognized finding that the overwhelming majority of patients with TTS are postmenopausal women, with a similar prevalence across ethnic groups, has been adding fuel to the concept that female sex hormones have an
important pathophysiologic role [2]. Indeed, experimental work has clearly demonstrated that estrogens exert various cardioprotective effects including inhibition of excessive sympatho-adrenal and renin–
angiotensin system activations as well as of antioxidant effects [3], thus suggesting that an estrogen deficiency, typical of the postmenopausal state, may be a predisposing factor of TTS. More than
3 decades after the original description of the condition, however, no clinical study has documented any association between sex hormone levels and TTS and the hormonal status of patients with TTS remains
poorly characterized [4]. Only Brenner et al., in 2012, assessed estradiol, progesterone, luteinizing hormone, and follicle-stimulating hormone in 17 women with TTS, 16 age-matched women with acute
myocardial infarction and 15 women with normal coronary arteries. These investigators found that the estradiol concentration at hospital admission was significantly higher in TTS patients than in the control groups, although this increase was transient and disappeared at follow-u
The progression of hypertrophic cardiomyopathy: dilatation of the left ventricle with supernormal systolic function
No full textWe performed cardiac catheterisation in a man who had been diagnosed as having hypertrophic cardiomyopathy 7 years earlier. The repeat angiogram showed the maintenance of a "supernormal" systolic function (ejection fraction: 87%) although there was an increase of left ventricular end-diastolic volume (from 65 to 132 ml/m2). This case suggests that progressive left ventricular dilatation should not necessarily be considered a marker of the progression of hypertrophic cardiomyopathy into a hypokinetic left ventricle
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