Bristow Lab

The Bristow Laboratory investigates chronic heart failure, specifically the molecular mechanisms involved in the genesis and progression of pathologic hypertrophy and contractile dysfunction that are hallmarks of this disease.  We measure myocardial gene expression in human clinical studies, and we also work with animal and cell models to gain an understanding of how gene expression changes relate to phenotypic changes and/or differences. More recently, based on previous work we did with the human heart ACE2 enzyme, we have added to the area of investigation mechanisms by which the SARS-CoV-2 virus attaches to, enters and damages myocardial cells.

Our studies correlating expression and phenotype have also allowed us to determine some of the genetic basis for the variability in therapeutic responses routinely observed for most classes of drugs, and these observations have been useful in the development of new pharmaceutical and device-based approaches to treat heart failure and other cardiovascular diseases. Over a more than 30 year period we have collected and processed diseased and control human heart samples from transplant and organ donor programs to create what is likely the largest tissue bank of its kind in the world. This tissue bank has proved extremely helpful in generating key hypotheses about important pathophysiological mechanisms, as well as in the discovery of genetic variants important in therapeutic responses.


Transcriptome signature of ventricular arrhythmias in dilated cardiomyopathy reveals increased fibrosis and activated TP53

Dynamic regulation of SARS-CoV-2 binding and cell entry mechanisms in remodeled human ventricular myocardium


GENETIC-AF: Bucindolol for the Maintenance of Sinus Rhythm in a Genotype-Defined Heart Failure Population.

A PDE3A Promoter Polymorphism Regulates cAMP-Induced Transcriptional Activity in Failing Human Myocardium.

Impact of Degree of Left Ventricular Remodeling on Clinical Outcomes From Cardiac Resynchronization Therapy.

Dose Response of β-Blockers in Adrenergic Receptor Polymorphism Genotypes.

Association of Variants in BAG3 With Cardiomyopathy Outcomes in African American Individuals.

Changing the Research Culture in the United States.

Improving Heart Failure Therapeutics Development in the United States: The Heart Failure Collaboratory.

Heart Rate in Preserved Ejection Fraction Heart Failure.

MicroRNAs in Heart Failure, Cardiac Transplantation, and Myocardial Recovery: Biomarkers with Therapeutic Potential.

Outcomes of cardiac resynchronization therapy in patients with intermittent atrial fibrillation or atrial flutter in the COMPANION trial.

Genetic variation expressed in the brain may impact heart failure. 

Myocardial microRNAs associated with reverse remodeling in human heart failure.


Fine Tuning Adenylyl Cyclase as a (Gene) Therapy for Heart Failure.

Data and Safety Monitoring Board evaluation and management of a renal adverse event signal in TOPCAT.

Reply: Is Histamine H2 Receptor a Real Promising Target for Prevention or Treatment of Heart Failure?

Histamine H2 Receptor Antagonists, Left Ventricular Morphology, and Heart Failure Risk: The MESA Study.


Sex-related differences in age-associated downregulation of human ventricular myocardial β1-adrenergic receptors.

The adrenergic system in pulmonary arterial hypertension: bench to bedside (2013 Grover Conference series).

Visual analysis of biological data-knowledge networks.

Cardiovascular drug development: is it dead or just hibernating?

Therapeutic Molecular Phenotype of β-Blocker-Associated Reverse-Remodeling in Nonischemic Dilated Cardiomyopathy.

Peax: interactive visual analysis and exploration of complex clinical phenotype and gene expression association.

Genetic variants are not associated with outcome in patients with coronary artery disease and left ventricular dysfunction: results of the Genetic Substudy of the Surgical Treatment for Ischemic Heart Failure (STICH) trials.

Change NIH/ Funding tab to say: Funding

  1. Training Faculty on 5T32HL007822-17, “Post Graduate Studies in Cardiovascular Research”, Buttrick P and Leinwand L, PIs
  2. AHA Strategically Focused Heart Failure Research Network (SFRN) grant titled, “A comprehensive approach to the treatment of heart failure with reduced ejection fraction (HFrEF)”, PI Peter Buttrick; PI for Project 2, “Therapeutic Molecular and Structural Phenotypic Changes of Heart Rate Reduction in HFrEF”
  3. AHA COVID-19 Rapid Response Award, M. Bristow PI.

Cardiology (SOM)

CU Anschutz

Anschutz Inpatient Pavilion 1

12605 East 16th Avenue

3rd Floor

Aurora, CO 80045


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