JAHA Accessed Jan 23, 2013
Review article
Showing posts with label Review. Show all posts
Showing posts with label Review. Show all posts
Wednesday, January 23, 2013
Sunday, March 18, 2012
PDE-5 inhibitors - Cardiac Uses
State-of-the-art Review: JACC 2012;59(1):9-15.
Bryan Schwartz et al.
Phosphodiesterase-5 inhibitors (PDE5Is) improve erectile function by enhancing nitric oxide availability in the penis and its supplying vasculature, resulting in vasodilation and increased blood flow. PDE5Is might benefit cardiovascular diseases because phosphodiesterase-5 is also located elsewhere in the body, including the pulmonary and systemic vasculature and in hypertrophied myocardium. PDE5Is are approved for pulmonary arterial hypertension, given that they improved several hemodynamic and clinical parameters in large randomized trials. Initial evidence suggests that PDE5Is benefit patients with congestive heart failure and secondary pulmonary hypertension. PDE5Is seem to improve hemodynamic and clinical parameters in patients with high-altitude pulmonary edema (HAPE) and high-altitude pulmonary hypertension. In climbers with prior episodes of HAPE, PDE5Is prevented HAPE in 2 small randomized trials. In small randomized trials of PDE5Is, patients with Raynaud's phenomenon demonstrated improved blood flow, fewer symptoms and frequency of attacks, and resolution of digital ulcers. In addition to enhancing vasodilation, PDE5Is seem to protect the myocardium through complex pathways that involve nitric oxide, cyclic guanosine monophosphate, protein kinase G, extracellular-signal-regulated kinase, B-cell lymphoma protein-2, and Rho kinase inhibition. In animal models of acute myocardial infarction, PDE5Is consistently reduced infarct size indicating cardioprotection and PDE5Is also promote reverse remodeling and reduce myocardial apoptosis, fibrosis, and hypertrophy. PDE5Is might also benefit patients with treatment-resistant hypertension, preeclampsia, or peripheral arterial disease. This review presents the pathophysiology and trial data with regard to the use of PDE5Is for cardiac diseases.
Tuesday, February 8, 2011
Genetics Primer for Primary Cardiologist
Circulation. 2011;123:544-550
Genetics Primer for the General Cardiologist. Impact of Genetic Insights Into Mendelian Disease on Cardiovascular Clinical Practice
Luke Kim, MD; Richard B. Devereux, MD; Craig T. Basson, MD, PhD
An extract of the first 250 words of the full text is provided, because this article has no abstract.
Introduction: Recent advances in the field of genetics have significantly enhanced our understanding of many cardiovascular conditions and improved diagnosis as well as management of these disorders. However, mendelian cardiovascular diseases still pose unique challenges to clinicians, especially when presented with inherited conditions that have a wide range of phenotypic presentations. In cardiovascular single-gene disorders with potentially devastating initial manifestations, such as sudden cardiac death (SCD) or aortic dissection, appropriate and prompt identification of individuals at risk is imperative. In addition, the management of the disease is not only applicable to the individuals at risk but also extends to other members in the family. Therefore, the general approach to patients with such diseases and their affected family members needs to be considered in the context of fundamental principles of mendelian inheritance. Numerous examples of cardiovascular mendelian disorders exist in which the importance of genetics has been clearly recognized, and most common monogenic cardiovascular disorders are transmitted in families in an autosomal dominant fashion. In such autosomal dominant disorders, it is important to remember the overriding principle that any first-degree relative of an individual with an autosomal dominant multigenerational familial cardiovascular disorder has a 50% chance of also being affected by this genetic trait. Thus, when added to a family history, any symptom or sign on history, clinical evaluation, or testing that is consistent with the diagnosis in question creates a >50% likelihood that the family member is affected by the disorder as well. In this review, we will focus on a . . . [Full Text of this Article]
Genetics Primer for the General Cardiologist. Impact of Genetic Insights Into Mendelian Disease on Cardiovascular Clinical Practice
Luke Kim, MD; Richard B. Devereux, MD; Craig T. Basson, MD, PhD
An extract of the first 250 words of the full text is provided, because this article has no abstract.
Introduction: Recent advances in the field of genetics have significantly enhanced our understanding of many cardiovascular conditions and improved diagnosis as well as management of these disorders. However, mendelian cardiovascular diseases still pose unique challenges to clinicians, especially when presented with inherited conditions that have a wide range of phenotypic presentations. In cardiovascular single-gene disorders with potentially devastating initial manifestations, such as sudden cardiac death (SCD) or aortic dissection, appropriate and prompt identification of individuals at risk is imperative. In addition, the management of the disease is not only applicable to the individuals at risk but also extends to other members in the family. Therefore, the general approach to patients with such diseases and their affected family members needs to be considered in the context of fundamental principles of mendelian inheritance. Numerous examples of cardiovascular mendelian disorders exist in which the importance of genetics has been clearly recognized, and most common monogenic cardiovascular disorders are transmitted in families in an autosomal dominant fashion. In such autosomal dominant disorders, it is important to remember the overriding principle that any first-degree relative of an individual with an autosomal dominant multigenerational familial cardiovascular disorder has a 50% chance of also being affected by this genetic trait. Thus, when added to a family history, any symptom or sign on history, clinical evaluation, or testing that is consistent with the diagnosis in question creates a >50% likelihood that the family member is affected by the disorder as well. In this review, we will focus on a . . . [Full Text of this Article]
Tuesday, January 11, 2011
Saturday, October 2, 2010
Iron Overload Cardiomyopathy - Review
Iron Overload Cardiomyopathy. Better understanding of an increasing disorder.
Pradeep Gujja, Douglas Rosing, Dorothy Tripoli, Yukitaka Shizukuda.
JACC 2010;56(13):1001-12.
Adult oriented. But, summarizes the current state and future directions in dealing with this disease. Useful read.
Tuesday, September 21, 2010
Troponin in Heart Failure - Review article (Adult)
J Am Coll Cardiol, 2010; 56:1071-1078
STATE-OF-THE-ART PAPER
Troponin Elevation in Heart Failure
Prevalence, Mechanisms, and Clinical Implications
Robb D. Kociol, MD*, Peter S. Pang, MD, Mihai Gheorghiade, MD, Gregg C. Fonarow, MD, Christopher M. O'Connor, MD* and G. Michael Felker, MD, MHS*,*
Circulating biomarkers have become increasingly important in diagnosing and risk stratifying patients with heart failure (HF). While the natriuretic peptides have received much focus, there is increasing interest in the role of circulating cardiac troponin (cTn) in detecting myocardial injury (often subclinical) in those with HF. Accumulating evidence suggests that patients with chronic and acute HF may have measurable levels of circulating cTn, whose detection and magnitude may have prognostic implications. Furthermore, as new, more sensitive cTn assays are being developed, larger numbers of HF patients are found to have detectable cTn with a persistent relationship between magnitude and outcome. This knowledge improves our ability to understand the mechanism of worsening HF, improve risk stratification, and detect potential injury related to new therapeutics in HF. As investigators begin to understand the relationship of detectable cTn to HF outcomes, as well as temporal changes in its magnitude, and its relationship to other circulating biomarkers, more insight may be gained into the progressive nature of cardiac dysfunction and the transition from chronic compensated to acute decompensated HF. Ultimately, this information might allow physicians to guide therapy, choose appropriate therapeutics, and improve HF outcomes.
STATE-OF-THE-ART PAPER
Troponin Elevation in Heart Failure
Prevalence, Mechanisms, and Clinical Implications
Robb D. Kociol, MD*, Peter S. Pang, MD, Mihai Gheorghiade, MD, Gregg C. Fonarow, MD, Christopher M. O'Connor, MD* and G. Michael Felker, MD, MHS*,*
Circulating biomarkers have become increasingly important in diagnosing and risk stratifying patients with heart failure (HF). While the natriuretic peptides have received much focus, there is increasing interest in the role of circulating cardiac troponin (cTn) in detecting myocardial injury (often subclinical) in those with HF. Accumulating evidence suggests that patients with chronic and acute HF may have measurable levels of circulating cTn, whose detection and magnitude may have prognostic implications. Furthermore, as new, more sensitive cTn assays are being developed, larger numbers of HF patients are found to have detectable cTn with a persistent relationship between magnitude and outcome. This knowledge improves our ability to understand the mechanism of worsening HF, improve risk stratification, and detect potential injury related to new therapeutics in HF. As investigators begin to understand the relationship of detectable cTn to HF outcomes, as well as temporal changes in its magnitude, and its relationship to other circulating biomarkers, more insight may be gained into the progressive nature of cardiac dysfunction and the transition from chronic compensated to acute decompensated HF. Ultimately, this information might allow physicians to guide therapy, choose appropriate therapeutics, and improve HF outcomes.
Thursday, July 8, 2010
Genetics: Genome Wide Association Studies - Review from NEJM
Article reviews the principles of the procedure and its implications.
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