Marc A. Pfeffer

Bio: Marc A. Pfeffer is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Heart failure & Myocardial infarction. The author has an hindex of 166, co-authored 765 publications receiving 133043 citations. Previous affiliations of Marc A. Pfeffer include Partners HealthCare & University of Miami.

Use of renin-angiotensin antagonist for reducing post myocardial infarct mobidity and mortality

Abstract: The invention involves a method for treating a human survivor of a heart attack and provides further improvement in survival following the heart attack by the early initiation and long-term administration of a renin-angiotensin system inhibitor, preferably an angiotensin converting enzyme inhibitor. The inhibitor may be used on its own, or in conjuction with other therapeutic compounds such as β blockers and thrombolytic agents. The preferred inhibitor is captopril.

Spironolactone effect on cardiac structure and function of patients with heart failure and preserved ejection fraction: a pooled analysis of three randomized trials

Abstract: Spironolactone is currently used in a large proportion of patients with heart failure and preserved ejection fraction (HFpEF), yet its effect on cardiac structure and function in a large population has not been well established. The aim of this study was to evaluate the impact of spironolactone on key echocardiographic parameters in HFpEF.

Review: Prospects for ARB in the next five years:

Abstract: JRAAS 2001;2:215-18 Based on multiple, well-conducted, randomised clinical outcome trials (RCT), inhibition of the renin-angiotensin system (RAS) with an angiotensin-converting enzyme inhibitor (ACE-I) has become a firmly established therapeutic approach for reducing morbidity and the risk of death across a broad spectrum of cardiovascular diseases (Figure 1). More recently, another pharmacologic class of agents that inhibits the RAS has become clinically available.Angiotensin II (Ang II) type 1 (AT1)-receptor blockers (ARBs) offer a more complete and specific way of inhibiting the actions of Ang II at the AT1-receptor. Unlike ACEI, ARBs do not directly interfere with the breakdown of bradykinin. When introduced, ARBs promised more complete inhibition of the RAS with greater efficacy and better tolerance than ACE-I. Although the better tolerance comparison appears to have been substantiated, the more important issue of clinical effectiveness of ARBs remains unsettled. We are fortunately in the midst of an impressive series of RCTs, which collectively will evaluate and quantitate the role of ARBs in clinical practice. Based on the ACE-I experience,we provide a framework to consider the completed and ongoing clinical outcomes RCTs with ARBs (Figure 2).

Infarct haemorrhage detected by cardiac magnetic resonance imaging: are we seeing the latest culprit in adverse left ventricular remodelling?

Abstract: > The force of the heart decreases … as the greater number of its parts become tendinous instead of fleshy. De sedibus et causus morborum > > G. B. Morgagni, 1761 All myocardial infarctions are not equal, and those that produce more extensive left ventricular topographical alterations are much more likely to result in premature morbidity and mortality. The advent of non-invasive cardiac imaging, particularly echocardiography, provided a temporal window to evaluate the dynamics of the structural alterations produced by a myocardial infarction. In the late 1970s, infarct expansion was defined as an acute dilatation and thinning of the infarcted region leading to an elongation of that segment which was not accounted for by further necrosis.1 This early change in ventricular contour often leading to an aneurysm identified patients at higher risk for early mortality and other infarct complications. In animal models, it became apparent that the early distortion of ventricular architecture in response to an extensive loss of myocytes was part of a more insidious progressive process of ventricular enlargement which involved the viable segment as well as the infarcted region. This architectural-modifying process termed ‘ventricular remodelling after myocardial infarction’ results in a larger ventricular chamber.2 Although the early enlargement may provide some compensation by restoring stroke volume despite a reduced ejection fraction, the alterations in left ventricular architecture create a chronic imbalance in loading conditions that leads to further topographic changes which augment risks for adverse events. Larger infarct size is the major factor promoting adverse left ventricular remodelling, and myocardial reperfusion performed during the myocyte salvage period remains the most definitive therapeutic modality to reduce adverse ventricular remodelling. Early studies also indicated that re-establishing coronary perfusion just outside of the window of salvage could still favourably attenuate some of the adverse structural changes by promoting prompter healing in the infarcted region.3 The complementary … *Corresponding author. Tel: +1 617 732 5500, Fax: +1 617 732 5291, E-mail: mapfeffer{at}bics.bwh.harvard.edu or mpfeffer{at}rics.bwh.harvard.edu

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.

Abstract: "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides a new guideline for hypertension prevention and management. The following are the key messages(1) In persons older than 50 years, systolic blood pressure (BP) of more than 140 mm Hg is a much more important cardiovascular disease (CVD) risk factor than diastolic BP; (2) The risk of CVD, beginning at 115/75 mm Hg, doubles with each increment of 20/10 mm Hg; individuals who are normotensive at 55 years of age have a 90% lifetime risk for developing hypertension; (3) Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent CVD; (4) Thiazide-type diuretics should be used in drug treatment for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes. Certain high-risk conditions are compelling indications for the initial use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, β-blockers, calcium channel blockers); (5) Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease); (6) If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic; and (7) The most effective therapy prescribed by the most careful clinician will control hypertension only if patients are motivated. Motivation improves when patients have positive experiences with and trust in the clinician. Empathy builds trust and is a potent motivator. Finally, in presenting these guidelines, the committee recognizes that the responsible physician's judgment remains paramount.

Cochrane Handbook for Systematic Reviews of Interventions

Abstract: The Cochrane Handbook for Systematic Reviews of Interventions is the official document that describes in detail the process of preparing and maintaining Cochrane systematic reviews on the effects of healthcare interventions.

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

A New Equation to Estimate Glomerular Filtration Rate

Abstract: The Modification of Diet in Renal Disease (MDRD) Study equation underestimates glomerular filtration rate (GFR) in patients with mild kidney disease. Levey and associates therefore developed and va...

Lifetime Prevalence and Age-of-Onset Distributions of DSM-IV Disorders in the National Comorbidity Survey Replication

Abstract: Context Little is known about lifetime prevalence or age of onset of DSM-IV disorders. Objective To estimate lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the recently completed National Comorbidity Survey Replication. Design and Setting Nationally representative face-to-face household survey conducted between February 2001 and April 2003 using the fully structured World Health Organization World Mental Health Survey version of the Composite International Diagnostic Interview. Participants Nine thousand two hundred eighty-two English-speaking respondents aged 18 years and older. Main Outcome Measures Lifetime DSM-IV anxiety, mood, impulse-control, and substance use disorders. Results Lifetime prevalence estimates are as follows: anxiety disorders, 28.8%; mood disorders, 20.8%; impulse-control disorders, 24.8%; substance use disorders, 14.6%; any disorder, 46.4%. Median age of onset is much earlier for anxiety (11 years) and impulse-control (11 years) disorders than for substance use (20 years) and mood (30 years) disorders. Half of all lifetime cases start by age 14 years and three fourths by age 24 years. Later onsets are mostly of comorbid conditions, with estimated lifetime risk of any disorder at age 75 years (50.8%) only slightly higher than observed lifetime prevalence (46.4%). Lifetime prevalence estimates are higher in recent cohorts than in earlier cohorts and have fairly stable intercohort differences across the life course that vary in substantively plausible ways among sociodemographic subgroups. Conclusions About half of Americans will meet the criteria for a DSM-IV disorder sometime in their life, with first onset usually in childhood or adolescence. Interventions aimed at prevention or early treatment need to focus on youth.