Plasma brain natriuretic peptide as a surrogate marker for cardioembolic stroke

<p>Abstract</p> <p>Background</p> <p>Cardioembolic stroke generally results in more severe disability, since it typically has a larger ischemic area than the other types of ischemic stroke. However, it is difficult to differentiate cardioembolic stroke from non-cardioembolic stroke (atherothrombotic stroke and lacunar stroke). In this study, we evaluated the levels of plasma brain natriuretic peptide in acute ischemic stroke patients with cardioembolic stroke or non-cardioembolic stroke, and assessed the prediction factors of plasma brain natriuretic peptide and whether we could differentiate between stroke subtypes on the basis of plasma brain natriuretic peptide concentrations in addition to patient's clinical variables.</p> <p>Methods</p> <p>Our patient cohort consisted of 131 consecutive patients with acute cerebral infarction who were admitted to Kagawa University School of Medicine Hospital from January 1, 2005 to December 31, 2007. The mean age of patients (43 females, 88 males) was 69.6 ± 10.1 years. Sixty-two patients had cardioembolic stroke; the remaining 69 patients had non-cardioembolic stroke (including atherothrombotic stroke, lacunar stroke, or the other). Clinical variables and the plasma brain natriuretic peptide were evaluated in all patients.</p> <p>Results</p> <p>Plasma brain natriuretic peptide was linearly associated with atrial fibrillation, heart failure, chronic renal failure, and left atrial diameter, independently (F_4,126= 27.6, p < 0.0001; adjusted R²= 0.45). Furthermore, atrial fibrillation, mitral regurgitation, plasma brain natriuretic peptide (> 77 pg/ml), and left atrial diameter (> 36 mm) were statistically significant independent predictors of cardioembolic stroke in the multivariable setting (Χ²= 127.5, p < 0.001).</p> <p>Conclusion</p> <p>It was suggested that cardioembolic stroke was strongly predicted with atrial fibrillation and plasma brain natriuretic peptide. Plasma brain natriuretic peptide can be a surrogate marker for cardioembolic stroke.</p

Troponin elevation in acute ischemic stroke (TRELAS) - protocol of a prospective observational trial

<p>Abstract</p> <p>Background</p> <p>Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.</p> <p>Methods/Design</p> <p>The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital Charité will be screened for cTnT elevations (i.e. >= 0.05 μg/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.</p> <p>Discussion</p> <p>TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.</p> <p>Trial registration</p> <p>clinicaltrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT01263964">NCT01263964</a></p

Cardiogenic shock with stunned myocardium during triple-h therapy treated with intra-aortic balloon pump counterpulsation

Excessive use of adrenergic agents may result in stunned myocardium.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Turkish registry for diagnosis and treatment of acute heart failure:

Objective: The goal of this study was to develop a national database of patients hospitalized in Turkey with acute heart failure (AHF) using evaluations of diagnostic and therapeutic approaches.Methods: Patient data were collected using an Internet-based survey. A total of 588 patients were enrolled from 36 participating medical centers across the country.Results: Mean age was 62 +/- 13 years and 38% of the patients were female. Ratio of de novo AHF to study cohort was 24%. Coronary heart disease and hypertension were found in 61% and 53% of the patients, respectively. Valvular heart disease was the underlying cause in 46% of heart failure patients. The most frequent factor associated with decompensation was noncompliance with treatment, observed in 34% of patients. Systolic blood pressure was 125 +/- 28 mmHg and heart rate was 93 +/- 22 beats/minute in the cohort. The most common findings on physical examination were inspiratory fine crackles (84%), peripheral edema (64%), and cold extremities in 34%. Mean ejection fraction (EF) measured at admission was 33 +/- 13%. Preserved EF (>=%40) was present in 20% of patients. On admission, 60%, 46%, and 40% of patients were using angiotens-in-converting enzyme inhibitor/angiotensin receptor blocker, beta-blocker, or aldosterone antagonist, respectively. In-hospital events were reported as 3.4% death, 1.6% stroke and 2% myocardial infarction.Conclusion: Compared to previous data collected around the world, AHF patients in Turkey were younger, had more frequently valvular heart disease as the underlying cause, and were more noncompliant with medical treatment, but overall mortality was lower. Drugs shown to reduce mortality, and which also form the basis of guideline-directed medical therapy, are still used inadequately