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Paula Dias

Publications and source records attributed to Paula Dias.

4 recordsLinked to original sources

B-type natriuretic peptide and left ventricular hypertrophy in hypertensive patients.

AIM: To assess the accuracy of B-type natriuretic peptide (BNP) plasma levels for the diagnosis of left ventricular hypertrophy (LVH) in hypertensive patients. PARTICIPANTS AND METHODS: We studied a sample of 409 adults aged 45 years or older, recruited from residents of Porto by random digit dialing. Data were collected by clinical interview and physical examination, ECG, echocardiogram and venous blood sampling for the measurement of plasma concentrations of BNP. Hypertension (HT) was defined as blood pressure > or = 140/90 mmHg on the day of interview and/or self-reported HT if treated with any antihypertensive medication; LVH was defined as left ventricular mass index (LVMI) > or = 125 g/m2 in men and 110 g/m2 in women. The participants were further classified in four strata according to left ventricular morphology--normal, concentric remodeling, eccentric LVH or concentric LVH. RESULTS: Two hundred and thirty-two (56.7%) individuals were hypertensive, and among these 73 (31.5%) had LVH. BNP levels were significantly higher in these individuals (median [P25-P75] = 55.8 pg/ml [22.6-88.4]) than in hypertensive patients without LVH (29.9 pg/ml [10.0-62.8]), p = 0.003. BNP levels also differed significantly across strata of left ventricular geometry, the main difference depending on the presence or absence of LVH. There was a positive correlation between plasma BNP levels and LVMI (Spearman's P 0.185, p = 0.005). The area under the ROC curve--a parameter for diagnostic accuracy quantification--was 0.62 (95% confidence interval 0.54-0.70), indicating low discriminatory power between normal and abnormal LVMI. CONCLUSION: In the assessed population, BNP levels were higher in hypertensive patients with LVH than in the absence of LVH. However, BNP did not perform well in discriminating between the presence or absence of LVH.

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Effect of a heart failure clinic on survival and hospital readmission in patients discharged from acute hospital care.

Ambulatory care by physicians especially devoted to the management of heart failure (HF) has been reported to have beneficial effects. The aim of this work was to assess the effect of outpatient management at a HF clinic, as compared with care by the usual assistant physician, on prognosis of HF patients. In this non-randomised study, we prospectively followed 339 patients after a hospitalisation index for HF, in order to compare prognosis between two groups of HF patients according to the ambulatory assistance setting: either a specific outpatient clinic (n=157) or the usual assistant physician (n=182). The outcomes assessed were all-cause death or cardiac-cause rehospitalisation during the first month after discharge and survival over the longer term. The risk of dying or being readmitted during the first month after discharge was significantly lower in patients followed at the HF clinic (adjusted odds ratio 0.23; 95% CI 0.12-0.46). Patients followed in the HF clinic also had an independent significantly lower hazard of dying during a longer-term follow up of average length 373 days (adjusted hazard ratio 0.52; 95% CI 0.34-0.81). The results support the fact that a multidisciplinary and permanently available medical staff might be of relevance in improving outcomes in HF patients.

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[Neurohumoral activation, regulation of sodium excretion and vasodilator treatment in heart insufficiency].

BACKGROUND: The benefits of vasodilator therapy guided by hemodynamic goals in patients with severe heart failure (HF) are well documented. Nevertheless, therapy induced arterial underfilling may activate compensatory neurohumoral mechanisms and sodium retention. OBJECTIVES: To evaluate the effect of vasodilator therapy on neurohumoral activation and sodium excretion in severe HF patients submitted to tailored therapy guided by hemodynamic parameters. METHODS: Ten male patients (aged 70.2 +/- 2.9 years) with severe HF (left ventricle ejection fraction = 15.2 +/- 1.1%) were evaluated according to hemodynamic parameters and plasma levels of brain natriuretic peptide (BNP), norepinephrine, aldosterone, plasma renin activity (PRA), sodium and creatinine and urinary levels of sodium and creatinine, prior to beginning of nitroprusside therapy, every six hours thereafter (for 24 hours) and again after five days of inhibition of angiotensin converting enzyme (ACE) with lisinopril. RESULTS: Nitroprusside therapy caused marked increase in cardiac index and substantial reduction in systemic vascular resistance index. Plasma levels of BNP failed significantly while those of PRA, aldosterone and norepinephrine markedly rose, causing substantial reduction of sodium urinary excretion. There were no changes in renal function. Following ACE inhibition by lisinopril, BNP and sodium plasma levels rose, but BNP values remained significantly lower than the initial ones. Norepinephrine and aldosterone returned to base levels and PRA rose sharply. There was an intense natriuretic response and significant elevation of urinary volume. Urinary creatinine and creatinine clearance decreased non-significantly. CONCLUSIONS: Our results show that intensive vasodilator therapy in patients with severe HF improves hemodynamic parameters and causes activation of renin-angiotensin-aldosterone and adrenergic systems, resulting in sodium retention. Nevertheless, this neurohumoral activation is reversed by ACE inhibitors, thus supporting the "wide spectrum" neurohumoral modulation role attributed to these drugs.

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Chronic left ventricular pseudoaneurism.

We present the case of a 70-year-old white male presenting with an abnormal cardiac silhouette on the chest X-ray and complaining of fatigue in the week before hospital admission. Four months before admission he had a single prolonged ischemic chest pain episode. The ECG revealed an old true posterior myocardial infarction. The transthoracic echocardiogram showed a large left ventricular pseudoaneurysm and surgical resection was performed successfully. The etiology, diagnosis and treatment of left ventricular pseudoaneurysm are reviewed.

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