• Imagen 1

Extracellular Cardiac Matrix Biomarkers in Patients With Acute Myocardial Infarction Complicated by Left Ventricular Dysfunction and Heart Failure. Insights From the Eplerenone Post-Acute Myocardial I

Circulation. 2009 Apr 27; Iraqi W, Rossignol P, Angioi M, Fay R, Nuée J, Ketelslegers JM, Vincent J, Pitt B, Zannad FBACKGROUND: -Aldosterone stimulates cardiac collagen synthesis. Circulating biomarkers of collagen turnover provide a useful tool for the assessment of cardiac remodeling in patients with congestive heart failure and left ventricular systolic dysfunction after acute myocardial infarction. Methods and Results-In a substudy of the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), which evaluated the effects of the selective aldosterone receptor antagonist eplerenone versus placebo, serum levels of collagen biomarkers were measured in 476 patients with congestive heart failure after acute myocardial infarction complicated with left ventricular systolic dysfunction. The combination of the type I collagen telopeptide and brain natriuretic peptide levels above median at baseline was associated with all-cause mortality and the composite end point of cardiovascular death or heart failure hospitalization, with hazard ratios of 2.49 (P=0.039) and 3.03 (P=0.002), respectively. During follow-up, levels of aminoterminal propeptide of type I and type III procollagen were found to be consistently lower in the eplerenone group and significantly lower beginning at 6 months. Conclusions-Changes in biomarkers of collagen synthesis and degradation suggest that extracellular matrix remodeling is an active process in patients with congestive heart failure and left ventricular systolic dysfunction after acute myocardial infarction. High type I collagen telopeptide and high brain natriuretic peptide serum levels are associated with the highest event rate. Eplerenone suppresses post-acute myocardial infarction collagen turnover changes.

Hypercalcemia: an evidence-based approach to clinical cases.

Iran J Kidney Dis. 2009 Apr; 3(2): 71-9Assadi FPrimary hyperparathyroidism and malignancy are responsible for greater than 90% of all cases of hypercalcemia. Compared with the hypercalcemia of malignancy, hyperparathyroidism tends to be associated with lower serum calcium levels (< 12 mg/dL) and a longer duration of hypercalcemia (more than 6 months). The hypercalcemic symptoms are usually fewer and subtle. Hyperparathyroidism tends to cause kidney calculi, hyperchloremic metabolic acidosis, and the characteristics of metabolic bone disease osteitis fibrosa cystica, but no anemia. In contrast, hypercalcemia of malignancy is typically rapid in onset, with higher serum calcium levels, and more severe symptoms. Patients so affected show marked anemia, but they never have kidney calculi or metabolic acidosis. Parathyroid hormone assay is the most useful test for differentiating hyperparathyroidism from malignancy and other causes of hypercalcemia. In hyperparathyroidism, serum parathyroid hormone levels will be elevated. In other cases, the high serum calcium concentration usually results in suppression of parathyroid hormone. Treatment of hypercalcemia should be started with hydration. Loop diuretics may be required in individuals with renal insufficiency or heart failure to prevent fluid overload. Calcitonin is administered for the immediate short-term management of severe symptomatic hypercalcemia. For long-term control of severe or symptomatic hypercalcemia, the addition of biphosphonate is typically required. Among intravenous bisphosphonates, zoledronic acid or pamidronate are the agents of choice. Glucocorticoids are effective in hypercalcemia due to lymphoma or granulomatous diseases. Dialysis is generally reserved for those with severe hypercalcemia complicated with kidney failure.

Plasma insulin-like growth factor I as predictor of progression and all cause mortality in chronic heart failure.

Growth Horm IGF Res. 2009 Apr 25; Andreassen M, Kistorp C, Raymond I, Hildebrandt P, Gustafsson F, Kristensen LO, Faber JOBJECTIVES: Insulin-like growth factor I (IGF-I) is an anabolic growth factor that seems to increase cardiac contractility. Reduced levels of IGF-I may be implicated in progression of CHF. The objective was to compare plasma IGF-I in CHF patients with healthy controls, and to examine the associations between baseline IGF-I levels, cardiac contractility and the prognosis as judged by all cause mortality and progression of CHF requiring admission to hospital. METHODS: A prospective study comprising 194 CHF outpatients, and 169 matched controls. All patients and controls underwent echocardiographic examination at baseline. Patients were followed for a median of 30months. RESULTS: There was no difference in IGF-I levels between patients and controls (median and interquartile range), 78 (58-91) vs. 77 (57-94)ng/mL (P=0.92). Age-adjusted IGF-I levels were not related to left ventricular ejection fraction (LVEF) (P=0.58) or levels of N-terminal B-Type natriuretic peptide (NT-proBNP) (P=0.42). During follow-up 44 patients died and 94 were admitted to hospital due to worsening of CHF. Adjusted for cardiovascular risk factors (age, gender, NT-proBNP, lipids, diabetes mellitus, blood pressure, renal function and LVEF) IGF-I levels did not influence the overall mortality risk or the admission rate to hospital, hazard ratio (HR) (95% confidence intervals) 1.05 (0.75-1.47) (P=0.77) and 1.00 (0.80-1.26) (P=0.96), respectively per each SD increase in log IGF-I levels. CONCLUSIONS: IGF-I levels were not reduced in patients with CHF and did not influence cardiac status at baseline or the prognosis.

The chance finding at multislice computed tomography coronary angiography of an ectopic origin of the left circumflex coronary artery from the right sinus of Valsalva.

Int J Cardiol. 2009 Apr 22; Dattilo G, Lamari A, Messina F, Imbalzano E, Salamone I, Carerj S, Marte F, Patanè SAnomalous coronary arteries occur in less than 2% of the general population. Most coronary anomalies are clinically asymptomatic. However some of them may present with chest pain, syncope, heart failure and sudden death. Acute myocardial infarction has been also described. Extravascular coronary compression results in dynamic obstruction which can cause effort angina as well as syncope and anomalous coronary arteries with an inter-arterial course are associated with sudden cardiac death. Anomalous origin of the circumflex coronary artery from the right sinus of Valsalva is thought to be of little clinical significance without the presence of severe narrowing of the vessel. Adequate visualization of the anomaly is essential for proper patient management. It has reported the full capability and accuracy of computed tomography coronary angiography in the identification and evaluation of the ectopic origin of the left circumflex coronary artery from the right sinus of Valsalva, displaying accurately the origin, size, course, and relationship of the anomalous vessel with respect to surrounding structures. We report a case of chance finding at multislice computed tomography coronary angiography of an ectopic origin of the left circumflex coronary artery from the right sinus of Valsalva. Also this case focuses attention on the anomalous origin of the circumflex coronary artery from the right sinus of Valsalva and confirms the full capability and accuracy of computed tomography coronary angiography in its adequate visualization.

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