Peter A McCullough

Texas Heart Institute, Houston, Texas, United States

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Publications (552)2830.34 Total impact

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    ABSTRACT: Background: Dialysis patients have high rates of cardiovascular morbidity and mortality, but data on arrhythmia burden, arrhythmia type, arrhythmia triggers, and the identity of terminal arrhythmias have historically been limited by an inability to monitor heart rhythm for prolonged periods. Objectives: To investigate arrhythmia and its association with sudden death in dialysis-dependent ESRD, describe the potential for implantable devices to advance study of dialysis physiology, review the ethical implications of using implantable devices in clinical studies, and report on the protocol and baseline results of the Monitoring in Dialysis Study (MiD). Design, setting, participants, & measurements: In this multicenter, interventional-observational, prospective cohort study, we placed implantable loop recorders in patients undergoing long-term hemodialysis. The proportion of patients experiencing clinically significant arrhythmias was the primary endpoint. For 6 months, we captured detailed data on the primary endpoint, symptomatic arrhythmias, other electrocardiographic variables, dialysis prescription, electrolytes, dialysis-related variables, and vital signs. We collected additional electrocardiographic data for up to 1 year. Results: Overall, 66 patients underwent implantation in sites in the United States and India. Diabetes was present in 63.6% of patients, 12.1% were age ≥70 years, 69.7% were men, and 53.0% were black. Primary and secondary endpoint data are expected in 2016. Conclusions: Cardiac arrhythmia is an important contributor to cardiovascular morbidity and mortality in dialysis patients, but available technology has previously limited the ability to estimate its true burden and triggers and to define terminal rhythms in sudden death. Use of implantable technology in observational studies raises complex issues but may greatly expand understanding of dialysis physiology. The use of implantable loop recorders in MiD is among the first examples of such a trial, and the results are expected to provide novel insights into the nature of arrhythmia in hemodialysis patients.
    No preview · Article · Jan 2016 · Clinical Journal of the American Society of Nephrology
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    ABSTRACT: Guideline-directed therapy for sepsis calls for early fluid resuscitation. Often patients receive large volumes of intravenous fluids. Bioimpedance vector analysis (BIVA) is a noninvasive technique useful for measuring total body water. In this prospective observational study, we enrolled 18 patients admitted to the intensive care unit for the treatment of sepsis syndromes. Laboratory data, clinical parameters, and BIVA were recorded daily. All but one patient experienced volume overload during the course of treatment. Two patients had >20 L of excess volume. Volume overload is clinically represented by tissue edema. Edema is not a benign condition, as it impairs tissue oxygenation, obstructs capillary blood flow, disrupts metabolite clearance, and alters cell-to-cell interactions. Specifically, volume overload has been shown to impair pulmonary, cardiac, and renal function. A positive fluid balance is a predictor of hospital mortality. As septic patients recover, volume excess should be aggressively treated with the use of targeted diuretics and renal replacement therapies if necessary.
    No preview · Article · Jan 2016 · Proceedings (Baylor University. Medical Center)
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    Mohammad Kazem Fallahzadeh · Peter A. McCullough

    Full-text · Article · Oct 2015 · American Journal of Nephrology

  • No preview · Article · Oct 2015 · Chest
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    Alberto Palazzuoli · Gaetano Ruocco · Claudio Ronco · Peter A McCullough
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    ABSTRACT: Current goals in the acute treatment of heart failure are focused on pulmonary and systemic decongestion with loop diuretics as the cornerstone of therapy. Despite rapid relief of symptoms in patients with acute decompensated heart failure, after intravenous use of loop diuretics, the use of these agents has been consistently associated with adverse events, including hypokalemia, azotemia, hypotension, and increased mortality. Two recent randomized trials have shown that continuous infusions of loop diuretics did not offer benefit but were associated with adverse events, including hyponatremia, prolonged hospital stay, and increased rate of readmissions. This is probably due to the limitations of congestion evaluation as well as to the deleterious effects linked to drug administration, particularly at higher dosage. The impaired renal function often associated with this treatment is not extensively explored and could deserve more specific studies. Several questions remain to be answered about the best diuretic modality administration, global clinical impact during acute and post-discharge period, and the role of renal function deterioration during treatment. Thus, if loop diuretics are a necessary part of the treatment for acute heart failure, then there must be an approach that allows personalization of therapy for optimal benefit and avoidance of adverse events.
    Full-text · Article · Sep 2015 · Critical care (London, England)
  • Yolanda Thompson-Martin · Peter A. McCullough · Varun Agrawal
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    ABSTRACT: Patients with chronic kidney disease (CKD) are often referred to a nephrologist late. Contributing factors include primary care providers' lack of awareness of practice guidelines for treating kidney disease and their uncertainty of timing for referral to a nephrologist. The purpose of this quasi-experimental study was to determine if advanced practice nurses working in primary care are knowledgeable about the National Kidney Foundations Kidney Disease Outcomes Quality Initiative Guidelines, if a CKD education program increases knowledge, and if knowledge is retained. Fourteen advanced practice nurses participated in the study. The knowledge outcome was measured using a CKD knowledge-based survey. The results showed a significant increase in knowledge post-intervention; moreover, knowledge gained was retained at the one-month follow-up interval. This evidence-based practice project was developed to promote timely referral to a nephrologist, which may then slow the progression of kidney disease, decrease morbidity and mortality, and reduce healthcare cost.
    No preview · Article · Sep 2015 · Nephrology nursing journal: journal of the American Nephrology Nurses' Association
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    ABSTRACT: The term cardiorenal syndrome (CRS) implies acute or chronic injury to the heart and kidneys that often involves a temporal sequence of disease initiation and progression. The classification of CRS is divided into five subtypes. Types 1 and 2 involve acute and chronic cardiovascular disease (CVD) scenarios leading to acute kidney injury (AKI) or accelerated chronic kidney disease (CKD). Types 3 and 4, describe AKI and CKD, respectively, leading primarily to heart failure, although, it is possible that acute coronary syndromes, stroke, and arrhythmias could be CVD outcomes in these forms of CRS. Finally, CRS type 5 describes a systemic insult to both heart and the kidneys, such as sepsis, where both organs are injured simultaneously in persons with previously normal heart and kidney function at baseline. This manuscript will summarize key issues and future opportunities in challenging patients with CRS. Because most CRS occur in patients with pre-existing myocardial disease or chronic kidney disease, we will emphasize the chronic condition which puts individuals at risk for acute events. In the setting of a hospitalization, acute CRS can occur which have been consistently associated with inpatient complications, longer lengths of intensive care unit and hospital stay, need for renal replacement therapy, rehospitalization and death. While there are several common diagnostic and therapeutic targets for the heart and kidney, there remains considerable opportunity for both in-vitro diagnostics and medicinal therapy to favorably influence the occurrence and natural history of CRS.
    Preview · Article · Sep 2015
  • Peter A. McCullough · Allan Young · William P. Shutze

    No preview · Article · Sep 2015 · JACC Cardiovascular Interventions

  • No preview · Article · Aug 2015
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    ABSTRACT: Hyperkalemia is defined as serum potassium concentrations elevated above the upper limit of normal (> 5.0 mEq/L). It has become more common in cardiovascular practice due to the growing population of patients with chronic kidney disease and the broad application of drugs that modulate renal elimination of potassium by reducing production of angiotensin II (angiotensin-converting enzyme inhibitors, direct renin inhibitors, β-adrenergic receptor antagonists), blocking angiotensin II receptors (angiotensin receptor blockers), or antagonizing the action of aldosterone on mineralocorticoid receptors (mineralocorticoid receptor antagonists). The risk of hyperkalemia is a major limiting factor for the use of these disease-modifying drugs in both acute and chronic cardiorenal syndromes. Thus, agents to control the plasma concentration of potassium are needed in the multidrug treatment of cardiorenal disease, including chronic kidney disease, heart failure, and acute kidney injury. Novel oral therapies in development for both acute and extended use in the management of hyperkalemia include patiromer sorbitex calcium and sodium zirconium cyclosilicate. Important biochemical differences between these compounds result in unique product profiles and electrolyte outcomes in patients treated for hyperkalemia. This review highlights the major mechanisms of hyperkalemia and key results from randomized trials in a range of clinical scenarios in patients with, and at risk for, hyperkalemia.
    No preview · Article · Jul 2015 · Reviews in cardiovascular medicine
  • Peter A McCullough · Gautam Patanker · Robert C Stoler

    No preview · Article · Jun 2015 · Journal of the American College of Cardiology
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    ABSTRACT: Over the past decade, science has greatly advanced our understanding of interdependent feedback mechanisms involving the heart, lung, and kidney. Organ injury is the consequence of maladaptive neurohormonal activation, oxidative stress, abnormal immune cell signaling, and a host of other mechanisms that precipitate adverse functional and structural changes. The presentation of interorgan crosstalk may include an acute, chronic, or acute on chronic timeframe. We review the current, state-of-the-art understanding of cardio-pulmonary-renal interactions and their related pathophysiology, perpetuating nature, and cycles of increased susceptibility and reciprocal progression. To this end, we present a multidisciplinary approach to frame the diverse spectrum of published observations on the topic. Assessment of organ functional reserve and use of biomarkers are valuable clinical strategies to screen and detect disease, assist in diagnosis, assess prognosis, and predict recovery or progression to chronic disease.
    Preview · Article · Jun 2015 · Journal of the American College of Cardiology
  • Alberto Palazzuoli · Peter A McCullough · Claudio Ronco · Ranuccio Nuti
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    ABSTRACT: Chronic kidney disease (CKD) in heart failure (HF) has been recognized as an independent risk factor for adverse outcome, although the most important clinical trials tend to exclude patients with moderate and severe renal insufficiency. Despite this common association, the precise pathophysiological connection and liaison between heart and kidney is partially understood. Moreover, is it not enough considering how much cardio-renal syndrome type 1 is attributable to previous CKD, and how much to new-onset acute kidney injury (AKI). Neither development of AKI, its progression and time nor duration is related to an adverse outcome. An AKI definition is not universally recognized, and many confounding terms have been used in literature: "worsening renal function", "renal impairment", "renal dysfunction", etc., are all names that contribute to misunderstanding, and do not facilitate an universal classification. Therefore, AKI development should be the consequence of the basal clinical characteristics of patients, different primitive kidney disease and hemodynamic status. AKI could also be the mirror of several underlying associated diseases poorly controlled. Finally, it is not clear which is the optimal laboratory tool for identifying patients with an increased risk of AKI. In the current report, we review the different kidney diseases' impact in HF, and we analyze the modalities for AKI recognition during HF focusing our attention about some new biomarkers with potential application in the current setting.
    No preview · Article · May 2015 · Internal and Emergency Medicine
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    ABSTRACT: Iloprost, a prostacyclin analogue, has been effective in preventing renal dysfunction among transplant patients. We hypothesized that iloprost is protective against renal dysfunction in different settings, in which similar underlying mechanisms of nephrotoxicity occur. We conducted a literature review, and discuss the application of iloprost in reducing acute renal insufficiency and the pathophysiological mechanisms of contrast-induced nephropathy (CIN). One proposed mechanism of CIN is prolonged renal arterial vasoconstriction, causing renal hypoperfusion, ischemia, and release of free radicals. Iloprost is an analogue of the vasodilatory prostaglandin PGI2 . It has demonstrated cytoprotective properties in the renal transplant population by inhibiting lysosomal degradation and release of free radicals, allowing membrane stabilization. Two good-quality studies reported on iloprost and CIN. Five studies reported protective effects of iloprost in renal transplantation and 1 in coronary artery bypass grafting. Iloprost was found to be renoprotective in patients with baseline renal insufficiency who underwent coronary angiography for CIN (risk ratio [RR] = 0.32, 95% confidence interval [CI]: 0.16-0.67) and increases the weighted mean difference improvement in creatinine clearance (RR = 4.56, 95% CI: 1.82-7.30). CIN is associated with major adverse cardiac events. Preventing CIN is important for patient safety and reducing disease burden. Iloprost may reduce CIN by up to 68%. The same mechanisms of iloprost that inhibit graft dysfunction in the acute post-renal transplant and cardiopulmonary bypass setting may also contribute to preventing CIN. Large randomized controlled trials are necessary to determine the clinical efficacy of iloprost in the angiography setting. © 2015 Wiley Periodicals, Inc.
    No preview · Article · May 2015 · Clinical Cardiology
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    ABSTRACT: Chronic kidney disease (CKD) is on the rise due to the increased rate of related comorbidities such as diabetes and hypertension. Patients with CKD are at higher risk of cardiovascular events and atrial fibrillation is more common in this patient population. It is estimated that the prevalence of chronic atrial fibrillation in patients with CKD is two to three times higher than general population. Furthermore, patients with CKD are less likely to stay in sinus rhythm. Atrial fibrillation presents a major burden in this population due to difficult treatment decisions in the setting of a lack of evidence from randomized clinical trials. Patients with CKD have higher risk of stroke with more than half having a CHADS2 score ≥ 2. Anticoagulation have been shown to significantly decrease embolic stroke risk, however bleeding complications such as hemorrhagic stroke is twofold higher with warfarin. Although newer novel anticoagulation drugs have shown promise with lower intracranial hemorrhage risk in comparison to warfarin, lack clinical trial data in CKD and the unavailability of an antidote remains an issue. In this review, we discuss the treatment options available including anticoagulation and the evidence behind them in patients with chronic kidney disease suffering from atrial fibrillation.
    No preview · Article · May 2015 · Journal of Atrial Fibrillation
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    ABSTRACT: The association between chronic kidney disease (CKD) and cardiovascular disease (CVD) is well established, and there is mounting evidence of interorgan cross talk that may accelerate pathologic processes and the progression of organ dysfunction in both systems. This process, termed cardiorenal syndrome (CRS) by the Acute Dialysis Quality Initiative, is considered a major health problem: patients with CKD and CVD are at much higher risk of mortality than patients with either condition alone. To date, the majority of CRS research has focused on neurohormonal mechanisms and hemodynamic alterations. However, mounting evidence suggests that abnormalities in the normal pathophysiology of the bone-mineral axis, iron, and erythropoietin play a role in accelerating CKD and CVD. The goal of this article is to review the role and interrelated effects of the bone-mineral axis and anemia in the pathogenesis of chronic CRS. Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    Full-text · Article · Feb 2015 · American Journal of Kidney Diseases
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    Peter A McCullough · Christina B Berberich

    Preview · Article · Jan 2015
  • Peter A McCullough · Ankit Mehta · Harold Szerlip

    No preview · Article · Dec 2014 · Journal of the American College of Cardiology
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    ABSTRACT: Objective: Neutrophil gelatinase-associated lipocalin (NGAL) is produced in response to tubular injury. Contrast-induced acute kidney injury (CI-AKI) is associated with adverse outcomes in chronic kidney disease (CKD) patients. We sought to characterize blood NGAL level and the degree of kidney injury in CKD patients who underwent coronary angiography. Methods: This study was a prospective, blinded assessment of blood samples obtained from patients with estimated glomerular filtration rates (eGFRs) between 15 and 90 mL/min/1.73 m2 undergoing elective coronary angiography with iodinated contrast. Blood NGAL and serum creatinine were measured at baseline, 1, 2, 4, 6, 12, 24 and 48 h after contrast administration. Results: A total of 63 subjects with a mean eGFR of 48.17±16.45 mL/min/1.73 m2 were enrolled. There was a graded increase in baseline NGAL levels across worsening stages of CKD (p=0.0001). Post-procedure NGAL increased from baseline in each stage of CKD. Eight (12.7%) patients were diagnosed with CI-AKI by diagnostic criteria of 2012 KDIGO definition of CI-AKI, and seven (11.1%) patients developed subclinical CI-AKI defined by a twofold or greater rise in NGAL. There was no relationship between baseline eGFR and diabetes on the composite outcome of subclinical and clinical CI-AKI. Conclusions: Baseline and post-procedure NGAL are progressively elevated according to the baseline stage of CKD. Using a twofold rise in NGAL, 46.7% of composite CI-AKI is detected and complements the 53.3% of cases identified using KDIGO criteria. Traditional risk predictors were not independently associated with this composite outcome.
    No preview · Article · Dec 2014 · Renal Failure
  • Timothy Ball · Kevin Wheelan · Peter A McCullough

    No preview · Article · Dec 2014 · Journal of the American College of Cardiology

Publication Stats

22k Citations
2,830.34 Total Impact Points


  • 2015
    • Texas Heart Institute
      Houston, Texas, United States
  • 2013-2015
    • Baylor University
      Waco, Texas, United States
    • St. John's Medical Center
      Jackson, Wyoming, United States
  • 2011-2015
    • Baylor Hamilton Heart and Vascular Hospital
      Dallas, Texas, United States
    • Northern New England Cardiovascular Research Study Group
      Lebanon, New Hampshire, United States
    • University of Missouri
      • Department of Internal Medicine
      Columbia, Missouri, United States
    • Cedars-Sinai Medical Center
      • Division of Cardiology
      Los Angeles, CA, United States
    • Oakland University
      Рочестер, Michigan, United States
  • 2010-2014
    • St. John Providence Health System
      Detroit, Michigan, United States
    • University of California, Los Angeles
      • Division of Cardiology
      Los Ángeles, California, United States
    • Paris Diderot University
      Lutetia Parisorum, Île-de-France, France
    • University of Alberta
      • Division of Critical Care Medicine
      Edmonton, Alberta, Canada
  • 2011-2013
    • Detroit Medical Center
      Detroit, Michigan, United States
  • 2010-2013
    • Providence Hospital
      Mobile, Alabama, United States
  • 2007-2013
    • The National Kidney Foundation
      New York, New York, United States
    • Wayne State University
      Detroit, Michigan, United States
    • University of Chicago
      • Department of Medicine
      Chicago, Illinois, United States
    • Columbia University
      New York, New York, United States
  • 2012
    • Saint Luke's Hospital (NY, USA)
      New York City, New York, United States
  • 2001-2012
    • University of Missouri - Kansas City
      • • "Saint Luke's" Mid America Heart Institute
      • • Department of Basic Med Sciences
      • • School of Medicine
      Kansas City, MO, United States
    • Albany Medical College
      • Division of Cardiology
      Albany, New York, United States
  • 1997-2012
    • William Beaumont Army Medical Center
      El Paso, Texas, United States
  • 2005-2010
    • Beaumont Health System
      • Department of Nutrition and Preventive Medicine
      Detroit, Michigan, United States
  • 2008
    • Eastern Virginia Medical School
      • School of Medicine
      Norfolk, VA, United States
  • 2006
    • Università degli Studi di Trieste
      Trst, Friuli Venezia Giulia, Italy
  • 2002-2006
    • University of Oslo
      • Division of Medicine
      Oslo, Oslo, Norway
  • 2001-2006
    • Truman Medical Center
      Kansas City, Kansas, United States
  • 2004
    • VA San Diego Healthcare System
      San Diego, California, United States
    • The Ohio State University
      Columbus, Ohio, United States
  • 1998-2004
    • Henry Ford Hospital
      • Department of Internal Medicine
      Detroit, Michigan, United States
  • 2003
    • National University (California)
      San Diego, California, United States
    • Duke University
      Durham, North Carolina, United States
    • Duke University Medical Center
      Durham, North Carolina, United States
    • Kansas City University of Medicine and Biosciences
      Kansas City, Missouri, United States
  • 1998-2003
    • Henry Ford Health System
      • Department of Emergency Medicine
      Detroit, Michigan, United States