Biomedical subjects

Paula Dias

Publications and source records attributed to Paula Dias.

6 recordsLinked to original sources

PubMed2006

Troponin I as a marker of right ventricular dysfunction and severity of pulmonary embolism.

BACKGROUND: Cardiac troponin I (cTnI) is a specific marker which allows detection of minor myocardial cell damage. In patients with severe pulmonary embolism (PE), the rise in pulmonary artery pressure can lead to progressive right ventricular dysfunction (RVD), and clinical studies have demonstrated the presence of ischemia and even right ventricular infarction. Our aims were to determine the prevalence and diagnostic utility of cTnI in identifying patients with RVD and to ascertain whether it correlates with severity of PE. METHODS: We studied 77 patients with PE diagnosed by pulmonary angiography, ventilation-perfusion lung scan, spiral computed tomography scan or a combination of abnormal echocardiogram with clinical presentation suggestive of PE or with positive subsidiary exams (d-dimers, venous Doppler of the lower limbs, ECG, blood gas analysis). We further classified the PE according to the European Society of Cardiology severity levels, the PE being: 1) massive, if there was shock and/or hypotension; 2) submassive, if we found right ventricular hypokinesis on the echocardiogram; and 3) non-massive, in the remaining cases. We considered the highest cTnI serum value from the admission to 24 hours and a normal value of < 0.10 ng/ml. RESULTS: Among the 60 patients with cTnI measurements, 42 had elevated values. Among those with RVD, 26 (81.3%) had increased cTnI levels and only 14 (35%) with elevated cTnI values did not have RVD, indicating that positive cTnI tests were significantly associated with RVD (p = 0.038). Patients with positive cTnI tests had earlier onset of symptoms (24.0 vs. 144.0 hours, p=0.02), higher prevalence of emboli in proximal vessels (pulmonary trunk and right or left main pulmonary arteries) (OR = 12, CI= 1.6-88.7), and received more thrombolytic therapy (OR = 5.4, CI = 1.1-26.8) than those with normal cTnI tests. cTnI levels were higher among patients with submassive PE (median: 0.77 ng/ml) and lower in those with non-massive PE (0.08 mg/ml, p < 0.05). CONCLUSIONS: Around 70% of patients with PE have elevated cTnI values and this test is significantly associated with RVD. cTnI measurements provide additional information in the evaluation of patients with PE by identifying more severe cases and those at increased risk of hemodynamic deterioration, who can benefit from more aggressive therapeutic strategies.

Biomarkers↗

PubMed2004

Prognostic information provided by serial measurements of brain natriuretic peptide in heart failure.

BACKGROUND: Brain natriuretic peptide (BNP) levels predict prognosis in heart failure patients. We aimed to evaluate if serial measurements of BNP can give additional prognostic information. METHODS: Eighty-four patients with systolic dysfunction had two measurements of BNP with an interval of 8 to 12 months and were followed in order to register the occurrence of death. The study was observational and prospectively designed. During follow-up, patients were treated according to state of the art. Physicians were kept blind to BNP levels. RESULTS: The median follow-up was 1190 days. The median initial BNP level was 260.4 pg/ml and decreased to 123 pg/ml in the second measurement (P=0.001). The decrease in BNP was significantly associated with ACE-i dosage and with the use of a beta-blocker. All-cause mortality was 20.2%. Patients whose initial BNP level was above the median had a significantly higher hazard of dying (HR 2.96, 95% CI 1.06-8.26). The same was observed for those whose BNP increased between the first and the second measurement (HR 2.64, 95% CI 1.00-7.00). In multivariable analysis, baseline BNP above the median and increasing BNP were associated with shorter survival. CONCLUSIONS: Higher baseline BNP and the increasing levels during follow-up were independently associated with mortality. The decrease in BNP levels was proportional to ACE-i dosage and larger among patients on beta-blockers. These results confirm the prognostic information provided by BNP determination and suggest that serial measurements give additional prognostic information.

Aged↗

PubMed2003

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.

Aged↗

PubMed2002

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.

Aged↗

PubMed2002

[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.

Aged↗

PubMed2002

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.

Aged↗